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class="ri-section"><div class="ri-section-header"><span>Interests</span></div><div class="ri-tags-container"><a data-click-track="profile-user-info-expand-research-interests" data-has-card-for-ri-list="37822776" href="https://www.academia.edu/Documents/in/Titanium"><div id="js-react-on-rails-context" style="display:none" data-rails-context="{"inMailer":false,"i18nLocale":"en","i18nDefaultLocale":"en","href":"https://independent.academia.edu/KarlokWong","location":"/KarlokWong","scheme":"https","host":"independent.academia.edu","port":null,"pathname":"/KarlokWong","search":null,"httpAcceptLanguage":null,"serverSide":false}"></div> <div class="js-react-on-rails-component" style="display:none" data-component-name="Pill" data-props="{"color":"gray","children":["Titanium"]}" data-trace="false" data-dom-id="Pill-react-component-c26e856d-20d6-4af3-97c0-4b5db0cb436f"></div> <div id="Pill-react-component-c26e856d-20d6-4af3-97c0-4b5db0cb436f"></div> </a><a 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class="right-panel-container"><div class="user-content-wrapper"><div class="uploads-container" id="social-redesign-work-container"><div class="upload-header"><h2 class="ds2-5-heading-sans-serif-xs">Uploads</h2></div><div class="documents-container backbone-social-profile-documents" style="width: 100%;"><div class="u-taCenter"></div><div class="profile--tab_content_container js-tab-pane tab-pane active" id="all"><div class="profile--tab_heading_container js-section-heading" data-section="Papers" id="Papers"><h3 class="profile--tab_heading_container">Papers by Kar-lok Wong</h3></div><div class="js-work-strip profile--work_container" data-work-id="17906364"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906364/Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model"><img alt="Research paper thumbnail of Preventive Treatment with Ketamine Attenuates the Ischaemia-Reperfusion Response in a Chronic Postischaemia Pain Model" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906364/Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model">Preventive Treatment with Ketamine Attenuates the Ischaemia-Reperfusion Response in a Chronic Postischaemia Pain Model</a></div><div class="wp-workCard_item"><span>Oxidative Medicine and Cellular Longevity</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome (CRPS). Ketamine has proposed anti-inflammatory effects and has been used for treating CRPS. This study aimed to evaluate anti-inflammatory and analgesic effects of ketamine after ischaemia-reperfusion injury in a chronic postischaemia pain (CPIP) model of CRPS-I. Using this model, ischemia was induced in the hindlimbs of male Sprague-Dawley rats. Ketamine, methylprednisolone, or saline was administered immediately after reperfusion. Physical effects, (oedema, temperature, and mechanical and cold allodynia) in the bilateral hindpaws, were assessed from 48 hours after reperfusion. Fewer (56%) rats in the ketamine group developed CPIP at the 48th hour after reperfusion (nonsignificant). Ketamine treated rats showed a significantly lower temperature in the ischaemic hindpaw compared to saline (P &amp;amp;amp;amp;amp;amp;amp;lt; 0.01) and methylprednisolone (P &amp;amp;amp;amp;amp;amp;amp;lt; 0.05) groups. Mechanical and cold allodynia were significantly lower in the ischaemic side in the ketamine group (P &amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Proinflammatory cytokines TNF-α and IL-2 were significantly lower at the 48th hour after reperfusion in ketamine and methylprednisolone groups, compared to saline (all P &amp;amp;amp;amp;amp;amp;amp;lt; 0.05). In conclusion, immediate administration of ketamine after an ischaemia-reperfusion injury can alleviate pain and inflammation in the CPIP model and has potential to treat postischaemic pain.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906364"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906364"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906364; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906364]").text(description); $(".js-view-count[data-work-id=17906364]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906364; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906364']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906364, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906364]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906364,"title":"Preventive Treatment with Ketamine Attenuates the Ischaemia-Reperfusion Response in a Chronic Postischaemia Pain Model","translated_title":"","metadata":{"abstract":"Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome (CRPS). Ketamine has proposed anti-inflammatory effects and has been used for treating CRPS. This study aimed to evaluate anti-inflammatory and analgesic effects of ketamine after ischaemia-reperfusion injury in a chronic postischaemia pain (CPIP) model of CRPS-I. Using this model, ischemia was induced in the hindlimbs of male Sprague-Dawley rats. Ketamine, methylprednisolone, or saline was administered immediately after reperfusion. Physical effects, (oedema, temperature, and mechanical and cold allodynia) in the bilateral hindpaws, were assessed from 48 hours after reperfusion. Fewer (56%) rats in the ketamine group developed CPIP at the 48th hour after reperfusion (nonsignificant). Ketamine treated rats showed a significantly lower temperature in the ischaemic hindpaw compared to saline (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.01) and methylprednisolone (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05) groups. Mechanical and cold allodynia were significantly lower in the ischaemic side in the ketamine group (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Proinflammatory cytokines TNF-α and IL-2 were significantly lower at the 48th hour after reperfusion in ketamine and methylprednisolone groups, compared to saline (all P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). In conclusion, immediate administration of ketamine after an ischaemia-reperfusion injury can alleviate pain and inflammation in the CPIP model and has potential to treat postischaemic pain.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"Oxidative Medicine and Cellular Longevity"},"translated_abstract":"Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome (CRPS). Ketamine has proposed anti-inflammatory effects and has been used for treating CRPS. This study aimed to evaluate anti-inflammatory and analgesic effects of ketamine after ischaemia-reperfusion injury in a chronic postischaemia pain (CPIP) model of CRPS-I. Using this model, ischemia was induced in the hindlimbs of male Sprague-Dawley rats. Ketamine, methylprednisolone, or saline was administered immediately after reperfusion. Physical effects, (oedema, temperature, and mechanical and cold allodynia) in the bilateral hindpaws, were assessed from 48 hours after reperfusion. Fewer (56%) rats in the ketamine group developed CPIP at the 48th hour after reperfusion (nonsignificant). Ketamine treated rats showed a significantly lower temperature in the ischaemic hindpaw compared to saline (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.01) and methylprednisolone (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05) groups. Mechanical and cold allodynia were significantly lower in the ischaemic side in the ketamine group (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Proinflammatory cytokines TNF-α and IL-2 were significantly lower at the 48th hour after reperfusion in ketamine and methylprednisolone groups, compared to saline (all P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). In conclusion, immediate administration of ketamine after an ischaemia-reperfusion injury can alleviate pain and inflammation in the CPIP model and has potential to treat postischaemic pain.","internal_url":"https://www.academia.edu/17906364/Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model","translated_internal_url":"","created_at":"2015-11-07T06:50:12.594-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906363"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906363/Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells"><img alt="Research paper thumbnail of Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906363/Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells">Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells</a></div><div class="wp-workCard_item"><span>European Journal of Pharmacology</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) con...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) concentration ([Ca(2+)]i) and is of prime importance in vascular tone regulation as NO relaxes vascular smooth muscle. Agonists could stimulate EC [Ca(2+)]i elevation by triggering Ca(2+) influx via plasma membrane ion channels, one of which is the store-operated Ca(2+) channel; the latter opens as a result of agonist-triggered internal Ca(2+) release. Endotoxin (lipopolysaccharide, LPS) could cause sepsis, which is often the fatal cause in critically ill patients. One of the LPS-induced damages is EC dysfunction, eventually leading to perturbations in hemodynamics. We obtained data showing that LPS-challenged mouse cerebral cortex endothelial bEND.3 cells did not suffer from apoptotic death, and in fact had intact agonist-triggered intracellular Ca(2+) release; however, they had reduced store-operated Ca(2+) entry (SOCE) after LPS treatment for 3h or more. Using real-time PCR, we did not find a decrease in gene expression of stromal interaction molecule 1 (STIM1) and Orai1 (two SOCE protein components) in bEND.3 cells treated with LPS for 15h. LPS inhibitory effects could be largely prevented by sodium salicylate (an inhibitor of nuclear factor-κB; NF-κB) or SB203580 (an inhibitor of p38 mitogen-activated protein kinases; p38 MAPK), suggesting that the p38 MAPK-NF-κB pathway is involved in SOCE inhibition.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906363"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906363"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906363; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906363]").text(description); $(".js-view-count[data-work-id=17906363]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906363; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906363']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906363, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906363]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906363,"title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells","translated_title":"","metadata":{"abstract":"Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) concentration ([Ca(2+)]i) and is of prime importance in vascular tone regulation as NO relaxes vascular smooth muscle. Agonists could stimulate EC [Ca(2+)]i elevation by triggering Ca(2+) influx via plasma membrane ion channels, one of which is the store-operated Ca(2+) channel; the latter opens as a result of agonist-triggered internal Ca(2+) release. Endotoxin (lipopolysaccharide, LPS) could cause sepsis, which is often the fatal cause in critically ill patients. One of the LPS-induced damages is EC dysfunction, eventually leading to perturbations in hemodynamics. We obtained data showing that LPS-challenged mouse cerebral cortex endothelial bEND.3 cells did not suffer from apoptotic death, and in fact had intact agonist-triggered intracellular Ca(2+) release; however, they had reduced store-operated Ca(2+) entry (SOCE) after LPS treatment for 3h or more. Using real-time PCR, we did not find a decrease in gene expression of stromal interaction molecule 1 (STIM1) and Orai1 (two SOCE protein components) in bEND.3 cells treated with LPS for 15h. LPS inhibitory effects could be largely prevented by sodium salicylate (an inhibitor of nuclear factor-κB; NF-κB) or SB203580 (an inhibitor of p38 mitogen-activated protein kinases; p38 MAPK), suggesting that the p38 MAPK-NF-κB pathway is involved in SOCE inhibition.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"European Journal of Pharmacology"},"translated_abstract":"Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) concentration ([Ca(2+)]i) and is of prime importance in vascular tone regulation as NO relaxes vascular smooth muscle. Agonists could stimulate EC [Ca(2+)]i elevation by triggering Ca(2+) influx via plasma membrane ion channels, one of which is the store-operated Ca(2+) channel; the latter opens as a result of agonist-triggered internal Ca(2+) release. Endotoxin (lipopolysaccharide, LPS) could cause sepsis, which is often the fatal cause in critically ill patients. One of the LPS-induced damages is EC dysfunction, eventually leading to perturbations in hemodynamics. We obtained data showing that LPS-challenged mouse cerebral cortex endothelial bEND.3 cells did not suffer from apoptotic death, and in fact had intact agonist-triggered intracellular Ca(2+) release; however, they had reduced store-operated Ca(2+) entry (SOCE) after LPS treatment for 3h or more. Using real-time PCR, we did not find a decrease in gene expression of stromal interaction molecule 1 (STIM1) and Orai1 (two SOCE protein components) in bEND.3 cells treated with LPS for 15h. LPS inhibitory effects could be largely prevented by sodium salicylate (an inhibitor of nuclear factor-κB; NF-κB) or SB203580 (an inhibitor of p38 mitogen-activated protein kinases; p38 MAPK), suggesting that the p38 MAPK-NF-κB pathway is involved in SOCE inhibition.","internal_url":"https://www.academia.edu/17906363/Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells","translated_internal_url":"","created_at":"2015-11-07T06:50:12.524-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010052,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":9493235,"co_author_invite_id":null,"email":"a***2@gmail.com","display_order":0,"name":"Tzu-hui su","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010060,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":4194304,"name":"Yuk-man Leung","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010078,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039504,"email":"m***g@mail.tku.edu.tw","display_order":6291456,"name":"Mei-ling Wang","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010088,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010099,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039509,"email":"z***u@sina.com.cn","display_order":7864320,"name":"Zhong-min Liu","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010100,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039510,"email":"l***u@cycu.edu.tw","display_order":8126464,"name":"Shyh-liang Lou","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010114,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039518,"email":"t***0@gmail.com","display_order":8257536,"name":"Tien-yao Tsai","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"}],"downloadable_attachments":[],"slug":"Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906361"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906361/Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes"><img alt="Research paper thumbnail of Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906361/Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes">Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes</a></div><div class="wp-workCard_item"><span>Pharmacological Reports</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also play an active role in modulating synaptic transmission. Palmitic acid (PA) is a saturated fatty acid which, when being excessive, is a significant risk factor for lipotoxicity. Activation of astrocytes by PA has been shown to cause neuronal inflammation and demyelination. However, direct damage by PA to astrocytes is relatively unexplored. The aim of this study was to identify the mechanism(s) of PA-induced cytotoxicity in rat cortical astrocytes and possible protection by (+)-catechin. Cytotoxicity and endoplasmic reticulum (ER) markers were assessed by MTT assay and Western blotting, respectively. Cytosolic Ca(2+) and mitochondrial membrane potential (MMP) were measured microfluorimetrically using fura-2 and rhodamine 123, respectively. Intracellular reactive oxygen species (ROS) production was assayed by the indicator 2&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-7&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorodihydrofluorescein diacetate. Exposure of astrocytes to 100μM PA for 24h resulted in apoptotic cell death. Whilst PA-induced cell death appeared to be unrelated to ER stress and perturbation in cytosolic Ca(2+) signaling, it was likely a result of ROS production and subsequent MMP collapse, since ascorbic acid (anti-oxidant, 100μM) prevented PA-induced MMP collapse and cell death. Co-treatment of astrocytes with (+)-catechin (300μM), an anti-oxidant found abundantly in green tea, significantly prevented PA-induced ROS production, MMP collapse and cell death. Our results suggest that PA-induced cytotoxicity in astrocytes may involve ROS generation and MMP collapse, which can be prevented by (+)-catechin.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906361"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906361"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906361; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906361]").text(description); $(".js-view-count[data-work-id=17906361]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906361; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906361']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906361, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906361]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906361,"title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes","translated_title":"","metadata":{"abstract":"Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also play an active role in modulating synaptic transmission. Palmitic acid (PA) is a saturated fatty acid which, when being excessive, is a significant risk factor for lipotoxicity. Activation of astrocytes by PA has been shown to cause neuronal inflammation and demyelination. However, direct damage by PA to astrocytes is relatively unexplored. The aim of this study was to identify the mechanism(s) of PA-induced cytotoxicity in rat cortical astrocytes and possible protection by (+)-catechin. Cytotoxicity and endoplasmic reticulum (ER) markers were assessed by MTT assay and Western blotting, respectively. Cytosolic Ca(2+) and mitochondrial membrane potential (MMP) were measured microfluorimetrically using fura-2 and rhodamine 123, respectively. Intracellular reactive oxygen species (ROS) production was assayed by the indicator 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorodihydrofluorescein diacetate. Exposure of astrocytes to 100μM PA for 24h resulted in apoptotic cell death. Whilst PA-induced cell death appeared to be unrelated to ER stress and perturbation in cytosolic Ca(2+) signaling, it was likely a result of ROS production and subsequent MMP collapse, since ascorbic acid (anti-oxidant, 100μM) prevented PA-induced MMP collapse and cell death. Co-treatment of astrocytes with (+)-catechin (300μM), an anti-oxidant found abundantly in green tea, significantly prevented PA-induced ROS production, MMP collapse and cell death. Our results suggest that PA-induced cytotoxicity in astrocytes may involve ROS generation and MMP collapse, which can be prevented by (+)-catechin.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Pharmacological Reports"},"translated_abstract":"Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also play an active role in modulating synaptic transmission. Palmitic acid (PA) is a saturated fatty acid which, when being excessive, is a significant risk factor for lipotoxicity. Activation of astrocytes by PA has been shown to cause neuronal inflammation and demyelination. However, direct damage by PA to astrocytes is relatively unexplored. The aim of this study was to identify the mechanism(s) of PA-induced cytotoxicity in rat cortical astrocytes and possible protection by (+)-catechin. Cytotoxicity and endoplasmic reticulum (ER) markers were assessed by MTT assay and Western blotting, respectively. Cytosolic Ca(2+) and mitochondrial membrane potential (MMP) were measured microfluorimetrically using fura-2 and rhodamine 123, respectively. Intracellular reactive oxygen species (ROS) production was assayed by the indicator 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorodihydrofluorescein diacetate. Exposure of astrocytes to 100μM PA for 24h resulted in apoptotic cell death. Whilst PA-induced cell death appeared to be unrelated to ER stress and perturbation in cytosolic Ca(2+) signaling, it was likely a result of ROS production and subsequent MMP collapse, since ascorbic acid (anti-oxidant, 100μM) prevented PA-induced MMP collapse and cell death. Co-treatment of astrocytes with (+)-catechin (300μM), an anti-oxidant found abundantly in green tea, significantly prevented PA-induced ROS production, MMP collapse and cell death. Our results suggest that PA-induced cytotoxicity in astrocytes may involve ROS generation and MMP collapse, which can be prevented by (+)-catechin.","internal_url":"https://www.academia.edu/17906361/Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes","translated_internal_url":"","created_at":"2015-11-07T06:50:12.350-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010045,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039500,"email":"d***u@mail.cmu.edu.tw","display_order":0,"name":"Dah-yuu Lu","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010051,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":9493235,"co_author_invite_id":null,"email":"a***2@gmail.com","display_order":4194304,"name":"Tzu-hui su","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010053,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":6291456,"name":"Yuk-man Leung","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010082,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010098,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039509,"email":"z***u@sina.com.cn","display_order":7864320,"name":"Zhong-min Liu","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010124,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039524,"email":"k***g@mail.cmu.edu.tw","display_order":8126464,"name":"Ka-shun Cheng","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010132,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039530,"email":"y***u@ms2.mmh.org.tw","display_order":8257536,"name":"Yu-ru Wu","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"}],"downloadable_attachments":[],"slug":"Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":9534,"name":"Calcium","url":"https://www.academia.edu/Documents/in/Calcium"},{"id":18459,"name":"Endoplasmic Reticulum Stress","url":"https://www.academia.edu/Documents/in/Endoplasmic_Reticulum_Stress"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":78467,"name":"Cerebral Cortex","url":"https://www.academia.edu/Documents/in/Cerebral_Cortex"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":196442,"name":"Astrocytes","url":"https://www.academia.edu/Documents/in/Astrocytes"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":1223957,"name":"Catechin","url":"https://www.academia.edu/Documents/in/Catechin"},{"id":1260596,"name":"Palmitic Acid","url":"https://www.academia.edu/Documents/in/Palmitic_Acid"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906360"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906360/Tetramethylpyrazine_Inhibits_Angiotensin_II_Increased_NAD_P_H_Oxidase_Activity_and_Subsequent_Proliferation_in_Rat_Aortic_Smooth_Muscle_Cells"><img alt="Research paper thumbnail of Tetramethylpyrazine Inhibits Angiotensin II-Increased NAD(P)H Oxidase Activity and Subsequent Proliferation in Rat Aortic Smooth Muscle Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/39773305/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906360/Tetramethylpyrazine_Inhibits_Angiotensin_II_Increased_NAD_P_H_Oxidase_Activity_and_Subsequent_Proliferation_in_Rat_Aortic_Smooth_Muscle_Cells">Tetramethylpyrazine Inhibits Angiotensin II-Increased NAD(P)H Oxidase Activity and Subsequent Proliferation in Rat Aortic Smooth Muscle Cells</a></div><div class="wp-workCard_item"><span>The American Journal of Chinese Medicine</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d16b3e949280e4d2457fd1af08e033b0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773305,"asset_id":17906360,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773305/download_file?st=MTczMjM3NDc1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906360"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906360"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906360; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906360]").text(description); $(".js-view-count[data-work-id=17906360]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906360; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906360']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906360, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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The aims of this study were to examine whether TMP may alter angiotenisn II (Ang II)-induced proliferation and to identify the putative underlying signaling pathways in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with TMP and then stimulated with Ang II, [ 3 H]-thymidine incorporation and the ET-1 expression was examined. Ang II increased DNA synthesis which was inhibited by TMP (1-100 µM). TMP inhibited the Ang II-induced ET-1 mRNA levels and ET-1 secretion. TMP also inhibited Ang II-increased NAD(P)H oxidase activity, intracellular reactive oxygen species (ROS) levels, and the ERK phosphorylation. Furthermore, TMP and antioxidants such as Trolox and diphenylene iodonium decreased Ang II-induced ERK phosphorylation, and activator protein-1 reporter activity. 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class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906359/Isosteviol_as_a_Potassium_Channel_Opener_to_Lower_Intracellular_Calcium_Concentrations_in_Cultured_Aortic_Smooth_Muscle_Cells">Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/TzhurngCheng">Tz-hurng Cheng</a></span></div><div class="wp-workCard_item"><span>Planta Medica</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly use...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly used as a non-caloric sugar substitute in Japan and Brazil. The present study attempted to elucidate the role of potassium (K (+)) channels in the action of isosteviol on intracellular calcium concentrations ([Ca (2+)]i) in cultured vascular smooth muscle (A7r5) cells using the Ca (2+)-sensitive dye Fura-2 as an indicator. The increase of [Ca (2+)]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by isosteviol from 0.01 micromol/L to 10 micromol/L. The attenuation by isosteviol of the vasopressin- and phenylephrine-induced increase in [Ca (2+)]i was inhibited by glibenclamide, apamin and 4-aminopyridine but not by charybdotoxin. Furthermore, the inhibitory action of isosteviol on [Ca (2+)]i was blocked when A7r5 cells co-treated with glibenclamide and apamin in conjunction with 4-aminopyridine were present. Therefore, not only did the ATP-sensitive potassium (K (ATP)) channel affect the action of isosteviol on [Ca (2+)]i modulation in A7r5 cells, but also those on the small conductance calcium-activated potassium (SK (Ca)) channels and voltage-gated (Kv) channels. However, the blockers of large-conductance Ca (2+)-activated potassium channels failed to modify the inhibitory action of isosteviol on [Ca (2+)]i. The obtained results indicated that a decrease of [Ca (2+)]i in A7r5 cells by isosteviol is mainly mediated by the selective opening of K (ATP) channel or/and SK (Ca) channel. Alteration in the Kv channel also plays a critical role in the inhibitory action of isosteviol.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906359"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906359"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906359; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906359]").text(description); $(".js-view-count[data-work-id=17906359]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906359; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906359']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906359, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906359]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906359,"title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells","translated_title":"","metadata":{"abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly used as a non-caloric sugar substitute in Japan and Brazil. The present study attempted to elucidate the role of potassium (K (+)) channels in the action of isosteviol on intracellular calcium concentrations ([Ca (2+)]i) in cultured vascular smooth muscle (A7r5) cells using the Ca (2+)-sensitive dye Fura-2 as an indicator. The increase of [Ca (2+)]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by isosteviol from 0.01 micromol/L to 10 micromol/L. The attenuation by isosteviol of the vasopressin- and phenylephrine-induced increase in [Ca (2+)]i was inhibited by glibenclamide, apamin and 4-aminopyridine but not by charybdotoxin. Furthermore, the inhibitory action of isosteviol on [Ca (2+)]i was blocked when A7r5 cells co-treated with glibenclamide and apamin in conjunction with 4-aminopyridine were present. Therefore, not only did the ATP-sensitive potassium (K (ATP)) channel affect the action of isosteviol on [Ca (2+)]i modulation in A7r5 cells, but also those on the small conductance calcium-activated potassium (SK (Ca)) channels and voltage-gated (Kv) channels. However, the blockers of large-conductance Ca (2+)-activated potassium channels failed to modify the inhibitory action of isosteviol on [Ca (2+)]i. The obtained results indicated that a decrease of [Ca (2+)]i in A7r5 cells by isosteviol is mainly mediated by the selective opening of K (ATP) channel or/and SK (Ca) channel. Alteration in the Kv channel also plays a critical role in the inhibitory action of isosteviol.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Planta Medica"},"translated_abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly used as a non-caloric sugar substitute in Japan and Brazil. The present study attempted to elucidate the role of potassium (K (+)) channels in the action of isosteviol on intracellular calcium concentrations ([Ca (2+)]i) in cultured vascular smooth muscle (A7r5) cells using the Ca (2+)-sensitive dye Fura-2 as an indicator. The increase of [Ca (2+)]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by isosteviol from 0.01 micromol/L to 10 micromol/L. The attenuation by isosteviol of the vasopressin- and phenylephrine-induced increase in [Ca (2+)]i was inhibited by glibenclamide, apamin and 4-aminopyridine but not by charybdotoxin. Furthermore, the inhibitory action of isosteviol on [Ca (2+)]i was blocked when A7r5 cells co-treated with glibenclamide and apamin in conjunction with 4-aminopyridine were present. Therefore, not only did the ATP-sensitive potassium (K (ATP)) channel affect the action of isosteviol on [Ca (2+)]i modulation in A7r5 cells, but also those on the small conductance calcium-activated potassium (SK (Ca)) channels and voltage-gated (Kv) channels. However, the blockers of large-conductance Ca (2+)-activated potassium channels failed to modify the inhibitory action of isosteviol on [Ca (2+)]i. The obtained results indicated that a decrease of [Ca (2+)]i in A7r5 cells by isosteviol is mainly mediated by the selective opening of K (ATP) channel or/and SK (Ca) channel. Alteration in the Kv channel also plays a critical role in the inhibitory action of isosteviol.","internal_url":"https://www.academia.edu/17906359/Isosteviol_as_a_Potassium_Channel_Opener_to_Lower_Intracellular_Calcium_Concentrations_in_Cultured_Aortic_Smooth_Muscle_Cells","translated_internal_url":"","created_at":"2015-11-07T06:50:12.171-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010039,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":118320,"email":"e***m@hindawi.com","display_order":0,"name":"I-min Liu","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010044,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":4194304,"name":"Juei-tang Cheng","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010067,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":37939559,"co_author_invite_id":836505,"email":"h***0@tmu.edu.tw","display_order":6291456,"name":"H.-h. Hsu","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010087,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010128,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":39564542,"co_author_invite_id":2039526,"email":"t***g@gate.sinica.edu.tw","display_order":7864320,"name":"Tz-hurng Cheng","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"}],"downloadable_attachments":[],"slug":"Isosteviol_as_a_Potassium_Channel_Opener_to_Lower_Intracellular_Calcium_Concentrations_in_Cultured_Aortic_Smooth_Muscle_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4083,"name":"Complementary and Alternative Medicine","url":"https://www.academia.edu/Documents/in/Complementary_and_Alternative_Medicine"},{"id":5541,"name":"Plant Biology","url":"https://www.academia.edu/Documents/in/Plant_Biology"},{"id":9534,"name":"Calcium","url":"https://www.academia.edu/Documents/in/Calcium"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":416452,"name":"Diterpenes","url":"https://www.academia.edu/Documents/in/Diterpenes"},{"id":521072,"name":"Stevia","url":"https://www.academia.edu/Documents/in/Stevia"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1134083,"name":"Medicinal Plant","url":"https://www.academia.edu/Documents/in/Medicinal_Plant"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906358"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906358/Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension"><img alt="Research paper thumbnail of Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906358/Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension">Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension</a></div><div class="wp-workCard_item"><span>Planta Medica</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (Compositae). It has been used popularly in Japan and Brazil as a sugar substitute for decades. Previous study has shown that it lowered blood pressure in spontaneously hypertensive rats (SHRs) when administered intravenously. This study shows that intraperitoneal injection of stevioside 25 mg/kg also has antihypertensive effect in SHRs. In isolated aortic rings from normal rats, stevioside could dose-dependently relax the vasopressin-induced vasoconstriction in both the presence and absence of endothelium. However, stevioside had no effect on phenylephrine- and KCl-induced phasic vasoconstriction. In addition, stevioside lost its influence on vasopressin-induced vasoconstriction in Ca(2+)-free medium. The results indicate that stevioside caused vasorelaxation via an inhibition of Ca(2+) influx into the blood vessel. This phenomenon was further confirmed in cultured aortic smooth muscle cells (A7r5). Using 10(-5) M methylene blue for 15 min, stevioside could still relax 10(-8) M vasopressin-induced vasoconstriction in isolated rat aortic rings, showing that this vasorelaxation effect was not related to nitric oxide. The present data show that the vasorelexation effect of stevioside was mediated mainly through Ca(2+) influx inhibition.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906358"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906358"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906358; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906358]").text(description); $(".js-view-count[data-work-id=17906358]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906358; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906358']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906358, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906358]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906358,"title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension","translated_title":"","metadata":{"abstract":"Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (Compositae). It has been used popularly in Japan and Brazil as a sugar substitute for decades. Previous study has shown that it lowered blood pressure in spontaneously hypertensive rats (SHRs) when administered intravenously. This study shows that intraperitoneal injection of stevioside 25 mg/kg also has antihypertensive effect in SHRs. In isolated aortic rings from normal rats, stevioside could dose-dependently relax the vasopressin-induced vasoconstriction in both the presence and absence of endothelium. However, stevioside had no effect on phenylephrine- and KCl-induced phasic vasoconstriction. In addition, stevioside lost its influence on vasopressin-induced vasoconstriction in Ca(2+)-free medium. The results indicate that stevioside caused vasorelaxation via an inhibition of Ca(2+) influx into the blood vessel. This phenomenon was further confirmed in cultured aortic smooth muscle cells (A7r5). Using 10(-5) M methylene blue for 15 min, stevioside could still relax 10(-8) M vasopressin-induced vasoconstriction in isolated rat aortic rings, showing that this vasorelaxation effect was not related to nitric oxide. The present data show that the vasorelexation effect of stevioside was mediated mainly through Ca(2+) influx inhibition.","publication_date":{"day":null,"month":null,"year":2001,"errors":{}},"publication_name":"Planta Medica"},"translated_abstract":"Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (Compositae). It has been used popularly in Japan and Brazil as a sugar substitute for decades. Previous study has shown that it lowered blood pressure in spontaneously hypertensive rats (SHRs) when administered intravenously. This study shows that intraperitoneal injection of stevioside 25 mg/kg also has antihypertensive effect in SHRs. In isolated aortic rings from normal rats, stevioside could dose-dependently relax the vasopressin-induced vasoconstriction in both the presence and absence of endothelium. However, stevioside had no effect on phenylephrine- and KCl-induced phasic vasoconstriction. In addition, stevioside lost its influence on vasopressin-induced vasoconstriction in Ca(2+)-free medium. The results indicate that stevioside caused vasorelaxation via an inhibition of Ca(2+) influx into the blood vessel. This phenomenon was further confirmed in cultured aortic smooth muscle cells (A7r5). Using 10(-5) M methylene blue for 15 min, stevioside could still relax 10(-8) M vasopressin-induced vasoconstriction in isolated rat aortic rings, showing that this vasorelaxation effect was not related to nitric oxide. The present data show that the vasorelexation effect of stevioside was mediated mainly through Ca(2+) influx inhibition.","internal_url":"https://www.academia.edu/17906358/Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension","translated_internal_url":"","created_at":"2015-11-07T06:50:12.084-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010041,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":0,"name":"Juei-tang Cheng","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"},{"id":9010083,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":4194304,"name":"Paul Chan","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"},{"id":9010097,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":38571549,"co_author_invite_id":414721,"email":"y***n@coh.org","display_order":6291456,"name":"Yi-jen Chen","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"},{"id":9010127,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":711477,"email":"l***6@knjc.edu.tw","display_order":7340032,"name":"Chun-nin Lee","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"}],"downloadable_attachments":[],"slug":"Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4083,"name":"Complementary and Alternative Medicine","url":"https://www.academia.edu/Documents/in/Complementary_and_Alternative_Medicine"},{"id":5541,"name":"Plant Biology","url":"https://www.academia.edu/Documents/in/Plant_Biology"},{"id":9534,"name":"Calcium","url":"https://www.academia.edu/Documents/in/Calcium"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":71399,"name":"Hypertension","url":"https://www.academia.edu/Documents/in/Hypertension"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":165799,"name":"Terpenes","url":"https://www.academia.edu/Documents/in/Terpenes"},{"id":194060,"name":"Asteraceae","url":"https://www.academia.edu/Documents/in/Asteraceae"},{"id":204388,"name":"Vasoconstriction","url":"https://www.academia.edu/Documents/in/Vasoconstriction"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":416452,"name":"Diterpenes","url":"https://www.academia.edu/Documents/in/Diterpenes"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1322750,"name":"Planta","url":"https://www.academia.edu/Documents/in/Planta"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906357"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906357/Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells"><img alt="Research paper thumbnail of Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906357/Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells">Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells</a></div><div class="wp-workCard_item"><span>Planta Medica</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective pro...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective properties. Not much is known about the effects of osthol on ionic channels, activities of which are implicated in vasorelaxation and neuroprotection. In this work we report that osthol could inhibit voltage-gated Na (+) currents with state-dependence in mouse neuroblastoma N2A cells (IC (50) = 12.3 microM and 31.5 microM at holding potentials of - 70 mV and - 100 mV, respectively). Current blockade was equally effective in both extracellular and intracellular application of osthol. Osthol (18 microM) did not significantly affect the kinetics and voltage-dependence of Na (+) channel activation, but left-shifted the steady-state inactivation curve (V (1/2) = - 60.5 mV and - 78.7 mV in the absence and presence of osthol, respectively). Osthol also mildly but significantly retarded channel recovery from inactivation (recovery time constant = 19.9 ms and 35.6 ms in the absence and presence of osthol, respectively). In addition, osthol blocked Na (+) currents in a frequency-dependent fashion: blockades of 17 %, 34 % and 49 % when currents were triggered at 0.33 Hz, 1 Hz and 3.33 Hz, respectively. Taken together, our results therefore suggest that osthol blocked voltage-gated Na (+) channels intracellularly with state- and frequency-dependence.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906357"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906357"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906357; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906357]").text(description); $(".js-view-count[data-work-id=17906357]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906357; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906357']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906357, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906357]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906357,"title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells","translated_title":"","metadata":{"abstract":"Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective properties. Not much is known about the effects of osthol on ionic channels, activities of which are implicated in vasorelaxation and neuroprotection. In this work we report that osthol could inhibit voltage-gated Na (+) currents with state-dependence in mouse neuroblastoma N2A cells (IC (50) = 12.3 microM and 31.5 microM at holding potentials of - 70 mV and - 100 mV, respectively). Current blockade was equally effective in both extracellular and intracellular application of osthol. Osthol (18 microM) did not significantly affect the kinetics and voltage-dependence of Na (+) channel activation, but left-shifted the steady-state inactivation curve (V (1/2) = - 60.5 mV and - 78.7 mV in the absence and presence of osthol, respectively). Osthol also mildly but significantly retarded channel recovery from inactivation (recovery time constant = 19.9 ms and 35.6 ms in the absence and presence of osthol, respectively). In addition, osthol blocked Na (+) currents in a frequency-dependent fashion: blockades of 17 %, 34 % and 49 % when currents were triggered at 0.33 Hz, 1 Hz and 3.33 Hz, respectively. Taken together, our results therefore suggest that osthol blocked voltage-gated Na (+) channels intracellularly with state- and frequency-dependence.","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"Planta Medica"},"translated_abstract":"Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective properties. Not much is known about the effects of osthol on ionic channels, activities of which are implicated in vasorelaxation and neuroprotection. In this work we report that osthol could inhibit voltage-gated Na (+) currents with state-dependence in mouse neuroblastoma N2A cells (IC (50) = 12.3 microM and 31.5 microM at holding potentials of - 70 mV and - 100 mV, respectively). Current blockade was equally effective in both extracellular and intracellular application of osthol. Osthol (18 microM) did not significantly affect the kinetics and voltage-dependence of Na (+) channel activation, but left-shifted the steady-state inactivation curve (V (1/2) = - 60.5 mV and - 78.7 mV in the absence and presence of osthol, respectively). Osthol also mildly but significantly retarded channel recovery from inactivation (recovery time constant = 19.9 ms and 35.6 ms in the absence and presence of osthol, respectively). In addition, osthol blocked Na (+) currents in a frequency-dependent fashion: blockades of 17 %, 34 % and 49 % when currents were triggered at 0.33 Hz, 1 Hz and 3.33 Hz, respectively. Taken together, our results therefore suggest that osthol blocked voltage-gated Na (+) channels intracellularly with state- and frequency-dependence.","internal_url":"https://www.academia.edu/17906357/Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.985-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010058,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":0,"name":"Yuk-man Leung","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010071,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":128927,"email":"k***h@mail.cmu.edu.tw","display_order":4194304,"name":"Yueh-hsiung Kuo","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010080,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":23641462,"co_author_invite_id":null,"email":"l***g@gmail.com","affiliation":"China Medical University,Taiwan","display_order":6291456,"name":"Li-Chi Chiang","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010096,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039508,"email":"u***7@cmu.edu.tw","display_order":7340032,"name":"Yi-huan Tsou","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010105,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039512,"email":"c***9@stsipa.gov.tw","display_order":7864320,"name":"Chun-hsiao Chou","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010116,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039519,"email":"c***o@twna.org.tw","display_order":8126464,"name":"Chia-chia Chao","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"}],"downloadable_attachments":[],"slug":"Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4083,"name":"Complementary and Alternative Medicine","url":"https://www.academia.edu/Documents/in/Complementary_and_Alternative_Medicine"},{"id":5541,"name":"Plant Biology","url":"https://www.academia.edu/Documents/in/Plant_Biology"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":256805,"name":"Neuroblastoma","url":"https://www.academia.edu/Documents/in/Neuroblastoma"},{"id":325790,"name":"Coumarins","url":"https://www.academia.edu/Documents/in/Coumarins"},{"id":361141,"name":"Angiosperms","url":"https://www.academia.edu/Documents/in/Angiosperms"},{"id":469018,"name":"Neoplasms","url":"https://www.academia.edu/Documents/in/Neoplasms"},{"id":470846,"name":"Voltage-Gated Sodium Channels","url":"https://www.academia.edu/Documents/in/Voltage-Gated_Sodium_Channels"},{"id":1953419,"name":"Neuroprotective Agents","url":"https://www.academia.edu/Documents/in/Neuroprotective_Agents"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906356"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906356/Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity"><img alt="Research paper thumbnail of Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906356/Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity">Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity</a></div><div class="wp-workCard_item"><span>Phytotherapy Research</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The purpose of this study was to investigate the antioxidant effects of a hot water extract of Pa...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The purpose of this study was to investigate the antioxidant effects of a hot water extract of Panax notoginseng (PNG) against chronic ethanol-induced hepatotoxicity. Fifty mice were divided into fi ve equal groups with 10 in each group. Group 1 (control) received saline, whereas group 2 received ethanol (70%, 0.1 mL, p.o.) once daily for 4 weeks, which induced hepatotoxicity, manifested biochemically by a significant elevation of serum enzyme activities, such as SGOT and SGPT. Hepatotoxicity was further evidenced by a significant increase in the hepatic lipid peroxidation measured. Groups 3-5 were administered a hot water extract of PNG at doses of 10, 25 and 50 mg/kg 2 weeks after initiating oral administration of ethanol, for a further 2 weeks. PNG ameliorated the rise in serum sGOT and sGPT induced by chronic ethanol administration. The mice were killed after PNG administration. In a separate study, PNG inhibited the lipid peroxidation in the mouse liver homogenate induced by ethanol in a dose-dependent manner. The findings indicate that PNG is an efficient cytoprotective agent against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen-free radicals that cause lipid peroxidation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906356"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906356"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906356; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906356]").text(description); $(".js-view-count[data-work-id=17906356]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906356; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906356']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906356, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906356]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906356,"title":"Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity","translated_title":"","metadata":{"abstract":"The purpose of this study was to investigate the antioxidant effects of a hot water extract of Panax notoginseng (PNG) against chronic ethanol-induced hepatotoxicity. Fifty mice were divided into fi ve equal groups with 10 in each group. Group 1 (control) received saline, whereas group 2 received ethanol (70%, 0.1 mL, p.o.) once daily for 4 weeks, which induced hepatotoxicity, manifested biochemically by a significant elevation of serum enzyme activities, such as SGOT and SGPT. Hepatotoxicity was further evidenced by a significant increase in the hepatic lipid peroxidation measured. Groups 3-5 were administered a hot water extract of PNG at doses of 10, 25 and 50 mg/kg 2 weeks after initiating oral administration of ethanol, for a further 2 weeks. PNG ameliorated the rise in serum sGOT and sGPT induced by chronic ethanol administration. The mice were killed after PNG administration. In a separate study, PNG inhibited the lipid peroxidation in the mouse liver homogenate induced by ethanol in a dose-dependent manner. The findings indicate that PNG is an efficient cytoprotective agent against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen-free radicals that cause lipid peroxidation.","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"Phytotherapy Research"},"translated_abstract":"The purpose of this study was to investigate the antioxidant effects of a hot water extract of Panax notoginseng (PNG) against chronic ethanol-induced hepatotoxicity. Fifty mice were divided into fi ve equal groups with 10 in each group. Group 1 (control) received saline, whereas group 2 received ethanol (70%, 0.1 mL, p.o.) once daily for 4 weeks, which induced hepatotoxicity, manifested biochemically by a significant elevation of serum enzyme activities, such as SGOT and SGPT. Hepatotoxicity was further evidenced by a significant increase in the hepatic lipid peroxidation measured. Groups 3-5 were administered a hot water extract of PNG at doses of 10, 25 and 50 mg/kg 2 weeks after initiating oral administration of ethanol, for a further 2 weeks. PNG ameliorated the rise in serum sGOT and sGPT induced by chronic ethanol administration. The mice were killed after PNG administration. In a separate study, PNG inhibited the lipid peroxidation in the mouse liver homogenate induced by ethanol in a dose-dependent manner. The findings indicate that PNG is an efficient cytoprotective agent against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen-free radicals that cause lipid peroxidation.","internal_url":"https://www.academia.edu/17906356/Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity","translated_internal_url":"","created_at":"2015-11-07T06:50:11.899-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010108,"work_id":17906356,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039515,"email":"c***6@uiuc.edu","display_order":0,"name":"Chi-feng Liu","title":"Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity"},{"id":9010125,"work_id":17906356,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039525,"email":"r***u@www.cmuh.org.tw","display_order":4194304,"name":"Rick Wu","title":"Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity"}],"downloadable_attachments":[],"slug":"Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":121705,"name":"Ethanol","url":"https://www.academia.edu/Documents/in/Ethanol"},{"id":260118,"name":"CHEMICAL SCIENCES","url":"https://www.academia.edu/Documents/in/CHEMICAL_SCIENCES"},{"id":269496,"name":"Panax","url":"https://www.academia.edu/Documents/in/Panax"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":1224429,"name":"Drug Induced Liver Injury","url":"https://www.academia.edu/Documents/in/Drug_Induced_Liver_Injury"},{"id":1473454,"name":"Liver function tests","url":"https://www.academia.edu/Documents/in/Liver_function_tests"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906355"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906355/Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity"><img alt="Research paper thumbnail of Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906355/Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity">Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity</a></div><div class="wp-workCard_item"><span>Phytotherapy Research</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect ag...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906355"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906355"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906355; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906355]").text(description); $(".js-view-count[data-work-id=17906355]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906355; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906355']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906355, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906355]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906355,"title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity","translated_title":"","metadata":{"abstract":"The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Phytotherapy Research"},"translated_abstract":"The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.","internal_url":"https://www.academia.edu/17906355/Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity","translated_internal_url":"","created_at":"2015-11-07T06:50:11.795-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010064,"work_id":17906355,"tagging_user_id":37822776,"tagged_user_id":37762182,"co_author_invite_id":null,"email":"l***g@ntnu.edu.tw","display_order":0,"name":"Li-ping Chang","title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity"},{"id":9010084,"work_id":17906355,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":4194304,"name":"Paul Chan","title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity"},{"id":9010110,"work_id":17906355,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039515,"email":"c***6@uiuc.edu","display_order":6291456,"name":"Chi-feng Liu","title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity"}],"downloadable_attachments":[],"slug":"Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":121705,"name":"Ethanol","url":"https://www.academia.edu/Documents/in/Ethanol"},{"id":233372,"name":"Lipid peroxidation","url":"https://www.academia.edu/Documents/in/Lipid_peroxidation"},{"id":260118,"name":"CHEMICAL SCIENCES","url":"https://www.academia.edu/Documents/in/CHEMICAL_SCIENCES"},{"id":290433,"name":"Antioxidant Activity","url":"https://www.academia.edu/Documents/in/Antioxidant_Activity"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":999291,"name":"Reishi","url":"https://www.academia.edu/Documents/in/Reishi"},{"id":1455811,"name":"Superoxides","url":"https://www.academia.edu/Documents/in/Superoxides"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906354"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906354/Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells"><img alt="Research paper thumbnail of Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906354/Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells">Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells</a></div><div class="wp-workCard_item"><span>Pharmacology</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly u...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. The aims of this study were to examine whether isosteviol alters angiotensin-II-induced cell proliferation in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with isosteviol, then stimulated with angiotensin II, after which [(3)H]thymidine incorporation and endothelin-1 secretion were examined. Isosteviol (1-100 micromol/l) inhibits angiotensin-II-induced DNA synthesis and endothelin-1 secretion. Measurements of 2&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;7&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorofluorescin diacetate, a redox-sensitive fluorescent dye, showed an isosteviol-mediated inhibition of intracellular reactive oxygen species generated by the effects of angiotensin II. The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine. In summary, we speculate that isosteviol inhibits angiotensin-II-induced cell proliferation and endothelin-1 secretion via attenuation of reactive oxygen species generation. Thus, this study provides important insights that may contribute to the effects of isosteviol on the cardiovascular system.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906354"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906354"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906354; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906354]").text(description); $(".js-view-count[data-work-id=17906354]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906354; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906354']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906354, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906354]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906354,"title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells","translated_title":"","metadata":{"abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. The aims of this study were to examine whether isosteviol alters angiotensin-II-induced cell proliferation in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with isosteviol, then stimulated with angiotensin II, after which [(3)H]thymidine incorporation and endothelin-1 secretion were examined. Isosteviol (1-100 micromol/l) inhibits angiotensin-II-induced DNA synthesis and endothelin-1 secretion. Measurements of 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorofluorescin diacetate, a redox-sensitive fluorescent dye, showed an isosteviol-mediated inhibition of intracellular reactive oxygen species generated by the effects of angiotensin II. The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine. In summary, we speculate that isosteviol inhibits angiotensin-II-induced cell proliferation and endothelin-1 secretion via attenuation of reactive oxygen species generation. Thus, this study provides important insights that may contribute to the effects of isosteviol on the cardiovascular system.","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"Pharmacology"},"translated_abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. The aims of this study were to examine whether isosteviol alters angiotensin-II-induced cell proliferation in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with isosteviol, then stimulated with angiotensin II, after which [(3)H]thymidine incorporation and endothelin-1 secretion were examined. Isosteviol (1-100 micromol/l) inhibits angiotensin-II-induced DNA synthesis and endothelin-1 secretion. Measurements of 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorofluorescin diacetate, a redox-sensitive fluorescent dye, showed an isosteviol-mediated inhibition of intracellular reactive oxygen species generated by the effects of angiotensin II. The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine. In summary, we speculate that isosteviol inhibits angiotensin-II-induced cell proliferation and endothelin-1 secretion via attenuation of reactive oxygen species generation. Thus, this study provides important insights that may contribute to the effects of isosteviol on the cardiovascular system.","internal_url":"https://www.academia.edu/17906354/Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.701-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010030,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1564394,"email":"j***n@mail.cmu.edu.tw","display_order":0,"name":"Jaung-geng Lin","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010031,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1054925,"email":"t***g@mail.cmu.edu.tw","display_order":4194304,"name":"Tzu-hurng Cheng","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010094,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":612359,"email":"w***u@tmu.edu.tw","display_order":6291456,"name":"Wen-ta Chiu","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010095,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039507,"email":"s***h@ndmctsgh.edu.tw","display_order":7340032,"name":"Shih-hurng Loh","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010101,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039511,"email":"h***y@tmu.edu.tw","display_order":7864320,"name":"Cheng-hsien Chen","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010122,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":40674726,"co_author_invite_id":1211305,"email":"l***2@ndmctsgh.edu.tw","display_order":8126464,"name":"Li-ling Lin","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"}],"downloadable_attachments":[],"slug":"Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":140,"name":"Pharmacology","url":"https://www.academia.edu/Documents/in/Pharmacology"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":312834,"name":"Cardiovascular system","url":"https://www.academia.edu/Documents/in/Cardiovascular_system"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":539690,"name":"Endothelin-1","url":"https://www.academia.edu/Documents/in/Endothelin-1"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":954841,"name":"Angiotensin II","url":"https://www.academia.edu/Documents/in/Angiotensin_II"},{"id":1455844,"name":"C-DNA Synthesis","url":"https://www.academia.edu/Documents/in/C-DNA_Synthesis"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17767103"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767103/Midazolam_induces_apoptosis_in_MA_10_mouse_Leydig_tumor_cells_through_caspase_activation_and_the_involvement_of_MAPK_signaling_pathway"><img alt="Research paper thumbnail of Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway" class="work-thumbnail" src="https://attachments.academia-assets.com/39698189/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767103/Midazolam_induces_apoptosis_in_MA_10_mouse_Leydig_tumor_cells_through_caspase_activation_and_the_involvement_of_MAPK_signaling_pathway">Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a></span></div><div class="wp-workCard_item"><span>OncoTargets and Therapy</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c22141809d786dde86742aad5595f034" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698189,"asset_id":17767103,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698189/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767103"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17767103"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17767103; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906353"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906353/Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat"><img alt="Research paper thumbnail of Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906353/Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat">Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly u...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. In the present study, the role of potassium channels in the vasodilator effect of isosteviol was investigated using potassium channel blockers on isosteviol-induced relaxation of isolated aortic rings prepared from Wistar rats. Isosteviol dose-dependently relaxed the vasopressin (10(-8) M)-induced vasoconstriction in isolated aortic rings with or without endothelium. However, in the presence of potassium chloride (3x10(-2) M), the vasodilator effect of isosteviol on arterial strips disappeared. Only the inhibitors specific for the ATP-sensitive potassium (K(ATP)) channel or small conductance calcium-activated potassium (SK(Ca)) channel inhibited the vasodilator effect of isosteviol in isolated aortic rings contracted with 10(-8) M vasopressin. Also; since the isosteviol-induced relaxation was unchanged by methylene blue, a role of nitric oxide and/or endothelium in the vasodilatation produced by isosteviol could be ruled out. The obtained results indicated that vasodilatation induced by isosteviol is related to the opening of SK(Ca) and K(ATP) channels.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906353"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906353"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906353; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906353]").text(description); $(".js-view-count[data-work-id=17906353]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906353; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906353']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906353, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906353]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906353,"title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat","translated_title":"","metadata":{"abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. In the present study, the role of potassium channels in the vasodilator effect of isosteviol was investigated using potassium channel blockers on isosteviol-induced relaxation of isolated aortic rings prepared from Wistar rats. Isosteviol dose-dependently relaxed the vasopressin (10(-8) M)-induced vasoconstriction in isolated aortic rings with or without endothelium. However, in the presence of potassium chloride (3x10(-2) M), the vasodilator effect of isosteviol on arterial strips disappeared. Only the inhibitors specific for the ATP-sensitive potassium (K(ATP)) channel or small conductance calcium-activated potassium (SK(Ca)) channel inhibited the vasodilator effect of isosteviol in isolated aortic rings contracted with 10(-8) M vasopressin. Also; since the isosteviol-induced relaxation was unchanged by methylene blue, a role of nitric oxide and/or endothelium in the vasodilatation produced by isosteviol could be ruled out. The obtained results indicated that vasodilatation induced by isosteviol is related to the opening of SK(Ca) and K(ATP) channels.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Life Sciences"},"translated_abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. In the present study, the role of potassium channels in the vasodilator effect of isosteviol was investigated using potassium channel blockers on isosteviol-induced relaxation of isolated aortic rings prepared from Wistar rats. Isosteviol dose-dependently relaxed the vasopressin (10(-8) M)-induced vasoconstriction in isolated aortic rings with or without endothelium. However, in the presence of potassium chloride (3x10(-2) M), the vasodilator effect of isosteviol on arterial strips disappeared. Only the inhibitors specific for the ATP-sensitive potassium (K(ATP)) channel or small conductance calcium-activated potassium (SK(Ca)) channel inhibited the vasodilator effect of isosteviol in isolated aortic rings contracted with 10(-8) M vasopressin. Also; since the isosteviol-induced relaxation was unchanged by methylene blue, a role of nitric oxide and/or endothelium in the vasodilatation produced by isosteviol could be ruled out. The obtained results indicated that vasodilatation induced by isosteviol is related to the opening of SK(Ca) and K(ATP) channels.","internal_url":"https://www.academia.edu/17906353/Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat","translated_internal_url":"","created_at":"2015-11-07T06:50:11.527-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010037,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":118320,"email":"e***m@hindawi.com","display_order":0,"name":"I-min Liu","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"},{"id":9010042,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":4194304,"name":"Juei-tang Cheng","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"},{"id":9010066,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":37939559,"co_author_invite_id":836505,"email":"h***0@tmu.edu.tw","display_order":6291456,"name":"H.-h. Hsu","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"},{"id":9010085,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"}],"downloadable_attachments":[],"slug":"Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":8014,"name":"Life Sciences","url":"https://www.academia.edu/Documents/in/Life_Sciences"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":138877,"name":"Vascular endothelium","url":"https://www.academia.edu/Documents/in/Vascular_endothelium"},{"id":160656,"name":"Potassium","url":"https://www.academia.edu/Documents/in/Potassium"},{"id":196381,"name":"Methylene Blue","url":"https://www.academia.edu/Documents/in/Methylene_Blue"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":416452,"name":"Diterpenes","url":"https://www.academia.edu/Documents/in/Diterpenes"},{"id":557691,"name":"Potassium Channels","url":"https://www.academia.edu/Documents/in/Potassium_Channels"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1035420,"name":"Vasodilation","url":"https://www.academia.edu/Documents/in/Vasodilation"},{"id":1295914,"name":"Potassium Chloride","url":"https://www.academia.edu/Documents/in/Potassium_Chloride"},{"id":1621878,"name":"Guanylate Cyclase","url":"https://www.academia.edu/Documents/in/Guanylate_Cyclase"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1724844,"name":"Molecular Structure","url":"https://www.academia.edu/Documents/in/Molecular_Structure"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906352"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906352/l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_"><img alt="Research paper thumbnail of l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906352/l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_">l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆</a></div><div class="wp-workCard_item"><span>The Journal of Nutritional Biochemistry</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provid...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provided by the blood stream; however, additional studies are needed to better understand the mechanism of L-carnitine supplementation to the heart. The aim of this study was to evaluate the effects of L-carnitine on angiotensin II (Ang II)-induced cardiac fibroblast proliferation and to explore its intracellular mechanism(s). Cultured rat cardiac fibroblasts were pretreated with L-carnitine (1-30 mM) then stimulated with Ang II (100 nM). Ang II increased fibroblast proliferation and endothelin-1 expression, which were partially inhibited by L-carnitine. L-carnitine also attenuated Ang II-induced NADPH oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, activator protein-1-mediated reporter activity and sphingosine-1-phosphate generation. In addition, L-carnitine increased prostacyclin (PGI(2)) generation in cardiac fibroblasts. siRNA transfection of PGI(2) synthase significantly reduced L-carnitine-induced PGI(2) and its anti-proliferation effects on cardiac fibroblasts. Furthermore, blockading potential PGI(2) receptors, including immunoprecipitation (IP) receptors and peroxisome proliferator-activated receptors alpha (PPAR alpha) and delta, revealed that siRNA-mediated blockage of PPAR alpha considerably reduced the anti-proliferation effect of L-carnitine. In summary, these results suggest that L-carnitine attenuates Ang II-induced effects (including NADPH oxidase activation, sphingosine-1-phosphate generation and cell proliferation) in part through PGI(2) and PPAR alpha-signaling pathways.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906352"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906352"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906352; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906352]").text(description); $(".js-view-count[data-work-id=17906352]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906352; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906352']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906352, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906352]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906352,"title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆","translated_title":"","metadata":{"abstract":"The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provided by the blood stream; however, additional studies are needed to better understand the mechanism of L-carnitine supplementation to the heart. The aim of this study was to evaluate the effects of L-carnitine on angiotensin II (Ang II)-induced cardiac fibroblast proliferation and to explore its intracellular mechanism(s). Cultured rat cardiac fibroblasts were pretreated with L-carnitine (1-30 mM) then stimulated with Ang II (100 nM). Ang II increased fibroblast proliferation and endothelin-1 expression, which were partially inhibited by L-carnitine. L-carnitine also attenuated Ang II-induced NADPH oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, activator protein-1-mediated reporter activity and sphingosine-1-phosphate generation. In addition, L-carnitine increased prostacyclin (PGI(2)) generation in cardiac fibroblasts. siRNA transfection of PGI(2) synthase significantly reduced L-carnitine-induced PGI(2) and its anti-proliferation effects on cardiac fibroblasts. Furthermore, blockading potential PGI(2) receptors, including immunoprecipitation (IP) receptors and peroxisome proliferator-activated receptors alpha (PPAR alpha) and delta, revealed that siRNA-mediated blockage of PPAR alpha considerably reduced the anti-proliferation effect of L-carnitine. In summary, these results suggest that L-carnitine attenuates Ang II-induced effects (including NADPH oxidase activation, sphingosine-1-phosphate generation and cell proliferation) in part through PGI(2) and PPAR alpha-signaling pathways.","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"The Journal of Nutritional Biochemistry"},"translated_abstract":"The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provided by the blood stream; however, additional studies are needed to better understand the mechanism of L-carnitine supplementation to the heart. The aim of this study was to evaluate the effects of L-carnitine on angiotensin II (Ang II)-induced cardiac fibroblast proliferation and to explore its intracellular mechanism(s). Cultured rat cardiac fibroblasts were pretreated with L-carnitine (1-30 mM) then stimulated with Ang II (100 nM). Ang II increased fibroblast proliferation and endothelin-1 expression, which were partially inhibited by L-carnitine. L-carnitine also attenuated Ang II-induced NADPH oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, activator protein-1-mediated reporter activity and sphingosine-1-phosphate generation. In addition, L-carnitine increased prostacyclin (PGI(2)) generation in cardiac fibroblasts. siRNA transfection of PGI(2) synthase significantly reduced L-carnitine-induced PGI(2) and its anti-proliferation effects on cardiac fibroblasts. Furthermore, blockading potential PGI(2) receptors, including immunoprecipitation (IP) receptors and peroxisome proliferator-activated receptors alpha (PPAR alpha) and delta, revealed that siRNA-mediated blockage of PPAR alpha considerably reduced the anti-proliferation effect of L-carnitine. In summary, these results suggest that L-carnitine attenuates Ang II-induced effects (including NADPH oxidase activation, sphingosine-1-phosphate generation and cell proliferation) in part through PGI(2) and PPAR alpha-signaling pathways.","internal_url":"https://www.academia.edu/17906352/l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_","translated_internal_url":"","created_at":"2015-11-07T06:50:11.436-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010035,"work_id":17906352,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1054925,"email":"t***g@mail.cmu.edu.tw","display_order":0,"name":"Tzu-hurng Cheng","title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆"},{"id":9010103,"work_id":17906352,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039511,"email":"h***y@tmu.edu.tw","display_order":4194304,"name":"Cheng-hsien Chen","title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆"},{"id":9010123,"work_id":17906352,"tagging_user_id":37822776,"tagged_user_id":40674726,"co_author_invite_id":1211305,"email":"l***2@ndmctsgh.edu.tw","display_order":6291456,"name":"Li-ling Lin","title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆"}],"downloadable_attachments":[],"slug":"l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":591,"name":"Nutrition and Dietetics","url":"https://www.academia.edu/Documents/in/Nutrition_and_Dietetics"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":131495,"name":"Heart","url":"https://www.academia.edu/Documents/in/Heart"},{"id":172083,"name":"Phosphorylation","url":"https://www.academia.edu/Documents/in/Phosphorylation"},{"id":234980,"name":"NADPH oxidase","url":"https://www.academia.edu/Documents/in/NADPH_oxidase"},{"id":295453,"name":"L-carnitine","url":"https://www.academia.edu/Documents/in/L-carnitine"},{"id":298041,"name":"Nutritional Biochemistry","url":"https://www.academia.edu/Documents/in/Nutritional_Biochemistry"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":392828,"name":"Myocardium","url":"https://www.academia.edu/Documents/in/Myocardium"},{"id":539690,"name":"Endothelin-1","url":"https://www.academia.edu/Documents/in/Endothelin-1"},{"id":573653,"name":"Food Sciences","url":"https://www.academia.edu/Documents/in/Food_Sciences"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":954841,"name":"Angiotensin II","url":"https://www.academia.edu/Documents/in/Angiotensin_II"},{"id":954995,"name":"Human Fibroblasts","url":"https://www.academia.edu/Documents/in/Human_Fibroblasts"},{"id":1361338,"name":"Sphingosine 1-phosphate","url":"https://www.academia.edu/Documents/in/Sphingosine_1-phosphate"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1763968,"name":"Gene Expression Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"},{"id":2003019,"name":"Sphingosine","url":"https://www.academia.edu/Documents/in/Sphingosine"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906351"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906351/Use_of_condoms_as_blade_covers_during_laryngoscopy_a_method_to_reduce_possible_cross_infection_among_patients"><img alt="Research paper thumbnail of Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients" class="work-thumbnail" src="https://attachments.academia-assets.com/39773303/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906351/Use_of_condoms_as_blade_covers_during_laryngoscopy_a_method_to_reduce_possible_cross_infection_among_patients">Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a></span></div><div class="wp-workCard_item"><span>Journal of Infection</span><span>, 2006</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="513fcbc9adf12945c5223b8056d564e7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773303,"asset_id":17906351,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773303/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906351"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906351"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906351; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906351]").text(description); $(".js-view-count[data-work-id=17906351]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906351; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906351']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906351, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "513fcbc9adf12945c5223b8056d564e7" } } $('.js-work-strip[data-work-id=17906351]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906351,"title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients","translated_title":"","metadata":{"grobid_abstract":"Objectives: Laryngoscope blades are in close contact with mucous membranes and can possibly contaminated with virulent or readily transmissible organisms. As laryngoscopy is often required during endotracheal intubation, proper cleaning and sterilization of the laryngoscope blade is crucial to prevent crosscontamination among patients. Methods: We tested the effectiveness of latex condom using as a laryngoscope blade cover during endotracheal intubation. Both control (no condom) and study group blades were rinsed with sterile saline after intubation. The rinse was sent for bacteria culture, and appearance of bacterial colonization was counted as positive. A water leak test (WLT) was performed on used condoms to verify their integrity. Results: There were total 162 laryngoscopes studied with 83 (51.2%) scopes in the study group and 79 (48.8%) in the control group. Rate of positive bacterial culture were 13.3% and 88.6% in the study and control group, respectively. Although WLT (C) rate of 41% was found in the study group, a high negative culture rate (71.6%) was also noted among the WLT (C) group. Conclusions: Condom when using as a blade cover during laryngoscopy is a simple, inexpansive and effective way in reducing cross contamination among patients.","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"Journal of Infection","grobid_abstract_attachment_id":39773303},"translated_abstract":null,"internal_url":"https://www.academia.edu/17906351/Use_of_condoms_as_blade_covers_during_laryngoscopy_a_method_to_reduce_possible_cross_infection_among_patients","translated_internal_url":"","created_at":"2015-11-07T06:50:11.342-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010028,"work_id":17906351,"tagging_user_id":37822776,"tagged_user_id":37925459,"co_author_invite_id":1975987,"email":"e***w@gmail.com","affiliation":"China Medical University,Taiwan","display_order":0,"name":"Edmund So","title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients"},{"id":9010076,"work_id":17906351,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1958426,"email":"c***h@hotmail.com","display_order":4194304,"name":"Yin-ching Chuang","title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients"},{"id":9010121,"work_id":17906351,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039523,"email":"y***g@mail.ukn.edu.tw","display_order":6291456,"name":"Yi-chueh Yang","title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among 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Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[{"id":39773303,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/39773303/thumbnails/1.jpg","file_name":"j.jinf.2005.03.004.pdf20151107-4773-122tvp8","download_url":"https://www.academia.edu/attachments/39773303/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Use_of_condoms_as_blade_covers_during_la.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/39773303/j.jinf.2005.03.004-libre.pdf20151107-4773-122tvp8?1446907895=\u0026response-content-disposition=attachment%3B+filename%3DUse_of_condoms_as_blade_covers_during_la.pdf\u0026Expires=1732272203\u0026Signature=DcRpLehFzxDSgmMCCP1eRD6YQdthZTP27bu24LqlNp8Y4woUyBHgdzgK2oMmGyz09wA3A4hKUH5xBiWWqhyDlAi8bpw7UwC912ZD5he-eu-kY8mzhz-DW6WvKSfrQml1WvT49hJ8k0Q5Vej5qSpR3R6kzzMg43dxXBpFcE-QtWgM0Y6OSFR0x0NiEQYRlyMJM~tJvInUrNmJIY1x9AegLURGtKx50w4xtIHjcE5KbftKknRZhXi0tCKbpjqv-VCts72gN7d8DRuhsTCDs7GLhft2hAE27szwZ-EJjL8ueD4noa-4JA1NOsNcU4N9dvmmhpWUxZVgSrrlxzYXu-9a4Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":55155,"name":"Emergency Medical Services","url":"https://www.academia.edu/Documents/in/Emergency_Medical_Services"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":109739,"name":"Infection","url":"https://www.academia.edu/Documents/in/Infection"},{"id":177876,"name":"Sterilization","url":"https://www.academia.edu/Documents/in/Sterilization"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":474853,"name":"Operating Rooms","url":"https://www.academia.edu/Documents/in/Operating_Rooms"},{"id":988244,"name":"Condoms","url":"https://www.academia.edu/Documents/in/Condoms"},{"id":1206482,"name":"Cross-infection","url":"https://www.academia.edu/Documents/in/Cross-infection"},{"id":1747358,"name":"Laryngoscopy","url":"https://www.academia.edu/Documents/in/Laryngoscopy"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906350"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906350/Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats"><img alt="Research paper thumbnail of Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906350/Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats">Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats</a></div><div class="wp-workCard_item"><span>Journal of Hypertension</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) receptor subtype, to investigate the effect of AT(1) receptor on the plasma glucose metabolism in streptozotocin-induced diabetic rats (STZ-diabetic rats). The plasma glucose concentration was assessed by glucose oxidase method and plasma insulin was measured using enzyme-linked immunosorbent assay. Systolic blood pressure (SBP) was determined by the tail-cuff method. The intravenous glucose challenge test (IVGCT) was carried out to evaluate the effect of valsartan on the glucose utilization in vivo. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis. Moreover, the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Plasma glucose-lowering action of valsartan also observed in normal rats although in a way not so effective as that in STZ-diabetic rats. Valsartan at the dose of 0.2 mg/kg that produced the maximal plasma glucose-lowering activity in STZ-diabetic rats is also effective to lower the SBP. However, oral treatment with nifedipine or nicorandil in STZ-diabetic rats at the dose sufficient to decrease SBP showed no change of plasma glucose. Otherwise, infusion of saralasin (10 microg/kg per min) into STZ-diabetic rats produced a plasma glucose-lowering activity similar to that by valsartan at 0.2 mg/kg. Moreover, valsartan (0.2 mg/kg) significantly attenuated the raise of plasma glucose induced by IVGCT in normal rats. Repeated intravenous administration of valsartan (0.2 mg/kg) in STZ-diabetic rats resulted in the lowering of plasma glucose after 3 days. The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days. Moreover, similar repeated treatment with valsartan reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. These results suggest that the plasma glucose-lowering activity of AT(1) receptor antagonism was associated with an increase in the glucose utilization in peripheral tissue and/or a reduction in hepatic gluconeogenesis in the absence of insulin.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906350"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906350"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906350; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906350]").text(description); $(".js-view-count[data-work-id=17906350]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906350; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906350']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906350, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906350]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906350,"title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats","translated_title":"","metadata":{"abstract":"In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) receptor subtype, to investigate the effect of AT(1) receptor on the plasma glucose metabolism in streptozotocin-induced diabetic rats (STZ-diabetic rats). The plasma glucose concentration was assessed by glucose oxidase method and plasma insulin was measured using enzyme-linked immunosorbent assay. Systolic blood pressure (SBP) was determined by the tail-cuff method. The intravenous glucose challenge test (IVGCT) was carried out to evaluate the effect of valsartan on the glucose utilization in vivo. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis. Moreover, the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Plasma glucose-lowering action of valsartan also observed in normal rats although in a way not so effective as that in STZ-diabetic rats. Valsartan at the dose of 0.2 mg/kg that produced the maximal plasma glucose-lowering activity in STZ-diabetic rats is also effective to lower the SBP. However, oral treatment with nifedipine or nicorandil in STZ-diabetic rats at the dose sufficient to decrease SBP showed no change of plasma glucose. Otherwise, infusion of saralasin (10 microg/kg per min) into STZ-diabetic rats produced a plasma glucose-lowering activity similar to that by valsartan at 0.2 mg/kg. Moreover, valsartan (0.2 mg/kg) significantly attenuated the raise of plasma glucose induced by IVGCT in normal rats. Repeated intravenous administration of valsartan (0.2 mg/kg) in STZ-diabetic rats resulted in the lowering of plasma glucose after 3 days. The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days. Moreover, similar repeated treatment with valsartan reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. These results suggest that the plasma glucose-lowering activity of AT(1) receptor antagonism was associated with an increase in the glucose utilization in peripheral tissue and/or a reduction in hepatic gluconeogenesis in the absence of insulin.","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"Journal of Hypertension"},"translated_abstract":"In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) receptor subtype, to investigate the effect of AT(1) receptor on the plasma glucose metabolism in streptozotocin-induced diabetic rats (STZ-diabetic rats). The plasma glucose concentration was assessed by glucose oxidase method and plasma insulin was measured using enzyme-linked immunosorbent assay. Systolic blood pressure (SBP) was determined by the tail-cuff method. The intravenous glucose challenge test (IVGCT) was carried out to evaluate the effect of valsartan on the glucose utilization in vivo. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis. Moreover, the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Plasma glucose-lowering action of valsartan also observed in normal rats although in a way not so effective as that in STZ-diabetic rats. Valsartan at the dose of 0.2 mg/kg that produced the maximal plasma glucose-lowering activity in STZ-diabetic rats is also effective to lower the SBP. However, oral treatment with nifedipine or nicorandil in STZ-diabetic rats at the dose sufficient to decrease SBP showed no change of plasma glucose. Otherwise, infusion of saralasin (10 microg/kg per min) into STZ-diabetic rats produced a plasma glucose-lowering activity similar to that by valsartan at 0.2 mg/kg. Moreover, valsartan (0.2 mg/kg) significantly attenuated the raise of plasma glucose induced by IVGCT in normal rats. Repeated intravenous administration of valsartan (0.2 mg/kg) in STZ-diabetic rats resulted in the lowering of plasma glucose after 3 days. The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days. Moreover, similar repeated treatment with valsartan reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. These results suggest that the plasma glucose-lowering activity of AT(1) receptor antagonism was associated with an increase in the glucose utilization in peripheral tissue and/or a reduction in hepatic gluconeogenesis in the absence of insulin.","internal_url":"https://www.academia.edu/17906350/Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats","translated_internal_url":"","created_at":"2015-11-07T06:50:11.266-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010036,"work_id":17906350,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":118320,"email":"e***m@hindawi.com","display_order":0,"name":"I-min Liu","title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats"},{"id":9010040,"work_id":17906350,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":4194304,"name":"Juei-tang Cheng","title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats"},{"id":9010081,"work_id":17906350,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":6291456,"name":"Paul Chan","title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats"}],"downloadable_attachments":[],"slug":"Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4228,"name":"Skeletal muscle biology","url":"https://www.academia.edu/Documents/in/Skeletal_muscle_biology"},{"id":27784,"name":"Gene expression","url":"https://www.academia.edu/Documents/in/Gene_expression"},{"id":71290,"name":"Hyperglycemia","url":"https://www.academia.edu/Documents/in/Hyperglycemia"},{"id":71300,"name":"Blood Glucose","url":"https://www.academia.edu/Documents/in/Blood_Glucose"},{"id":71399,"name":"Hypertension","url":"https://www.academia.edu/Documents/in/Hypertension"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":790002,"name":"Streptozotocin","url":"https://www.academia.edu/Documents/in/Streptozotocin"},{"id":901298,"name":"Glucose Tolerance Test","url":"https://www.academia.edu/Documents/in/Glucose_Tolerance_Test"},{"id":915951,"name":"Type 2 Diabetes Mellitus","url":"https://www.academia.edu/Documents/in/Type_2_Diabetes_Mellitus"},{"id":1029499,"name":"Nifedipine","url":"https://www.academia.edu/Documents/in/Nifedipine"},{"id":1031967,"name":"Diabetic Rat","url":"https://www.academia.edu/Documents/in/Diabetic_Rat"},{"id":1954221,"name":"Calcium Channel Blockers","url":"https://www.academia.edu/Documents/in/Calcium_Channel_Blockers"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906349"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906349/Hypoxia_induced_matrix_metalloproteinase_13_expression_in_astrocytes_enhances_permeability_of_brain_endothelial_cells"><img alt="Research paper thumbnail of Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells" class="work-thumbnail" src="https://attachments.academia-assets.com/39773304/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906349/Hypoxia_induced_matrix_metalloproteinase_13_expression_in_astrocytes_enhances_permeability_of_brain_endothelial_cells">Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells</a></div><div class="wp-workCard_item"><span>Journal of Cellular Physiology</span><span>, 2009</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7622911da6d8dd4616b7cba16edb9dd6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773304,"asset_id":17906349,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773304/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906349"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906349"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906349; 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Here we found that hypoxia increased MMP-13 protein and mRNA levels in primary rat astrocyte cultures. Hypoxia stimulation also increased the secretion of MMP-13 from astrocytes, as shown by zymographic analysis. In addition, exposure to hypoxia up-regulated the expression of c-Fos and c-Jun time-dependently. Hypoxia-induced MMP-13 overexpression was antagonized by transfection with antisense oligodeoxynucleotides (AS-ODN) of c-Fos or c-Jun. Furthermore, hypoxic-conditioned medium (Hx-CM) collected from astrocytes exposed to hypoxia increased paracellular permeability of adult rat brain endothelial cells (ARBECs). Administration of MMP-13 neutralizing antibody antagonized Hx-CM-induced paracellular permeability of ARBECs. Furthermore, pre-transfection of astrocytes with AS-ODN of c-Fos, c-Jun or MMP-13-shRNA significantly decreased hyperpermeability of ARBECs induced by Hx-CM. The arrangement of tight junction protein (TJP) zonular occludens-1 (ZO-1) of ARBECs disorganized in response to Hx-CM. Administration of Hx-CM to ARBECs also resulted in the production of proteolytic fragments of ZO-1, which was antagonized by transfection of MMP-13-shRNA in primary astrocytes. Administration of MMP-13 recombinant protein to ARBECs led to the disorganization and fragmentation of ZO-1 protein and also increased paracellular permeability. These results suggest that hypoxia-induced MMP-13 expression in astrocytes is regulated by c-Fos and c-Jun. MMP-13 is an important factor leading to the disorganization of ZO-1 and hyperpermeablility of blood-brain barrier in response to hypoxia.","publication_date":{"day":null,"month":null,"year":2009,"errors":{}},"publication_name":"Journal of Cellular Physiology","grobid_abstract_attachment_id":39773304},"translated_abstract":null,"internal_url":"https://www.academia.edu/17906349/Hypoxia_induced_matrix_metalloproteinase_13_expression_in_astrocytes_enhances_permeability_of_brain_endothelial_cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.184-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010048,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039500,"email":"d***u@mail.cmu.edu.tw","display_order":0,"name":"Dah-yuu Lu","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells"},{"id":9010057,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":4194304,"name":"Yuk-man Leung","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells"},{"id":9010072,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1946164,"email":"c***l@mail.cmu.edu.tw","display_order":6291456,"name":"Chih-ho Lai","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells"},{"id":9010074,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":263183925,"co_author_invite_id":2039502,"email":"w***i@ntu.edu.tw","display_order":7340032,"name":"Wen-mei Fu","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906348"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906348/Bradykinin_induced_cell_migration_and_COX_2_production_mediated_by_the_bradykinin_B1_receptor_in_glioma_cells"><img alt="Research paper thumbnail of Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells" class="work-thumbnail" src="https://attachments.academia-assets.com/39773302/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906348/Bradykinin_induced_cell_migration_and_COX_2_production_mediated_by_the_bradykinin_B1_receptor_in_glioma_cells">Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells</a></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2010</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1b4988d1e3b70267e8782e9aad6a1870" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773302,"asset_id":17906348,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773302/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: 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var workId = 17906348; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906348']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906348, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher 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Recent reports have also shown that bradykinin selectively modulates blood-tumor barrier permeability. However, the molecular mechanisms and pathologic roles underlying bradykinin-induced glioma migration remain unclear. Glioma is the most common primary adult brain tumor, with a poor prognosis because of the ease with which tumor cells spread to other regions of the brain. In this study, we found that bradykinin increases the cell migration and expression of cyclooxygenase-2 (COX-2) in glioma cells. Bradykinin-mediated migration was attenuated by the selective COX-2 inhibitor NS-398. Moreover, increased motility of glioma cells and expression of COX-2 were mimicked by a bradykinin B1 receptor (B1R) agonist and markedly inhibited by a B1R antagonist. Bradykinin-mediated migration was attenuated by phosphoinositide 3-kinase (PI-3 kinase)/AKT inhibitors LY 294002 and wortmannin. Bradykinin stimulation also increased the phosphorylation of the p85 subunit of PI-3 kinase and serine 473 of AKT. Treatment of bradykinin with AP-1 inhibitors Tanshinone IIA and curcumin also reduced COX-2 expression and glioma cell migration. Moreover, treatment of bradykinin also induced phosphorylation of c-Jun in glioma cells. AP-1 promoter analysis in the luciferase reporter construct showed that bradykinin increased AP-1 transcription activity and was inhibited by LY 294002 and wortmannin. One mechanism underlying bradykinin-directed migration is transcriptional up-regulation of COX-2 and activation of the B1R receptor, PI-3 kinase, AKT, c-Jun, and AP-1 pathways.","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"Journal of Cellular Biochemistry","grobid_abstract_attachment_id":39773302},"translated_abstract":null,"internal_url":"https://www.academia.edu/17906348/Bradykinin_induced_cell_migration_and_COX_2_production_mediated_by_the_bradykinin_B1_receptor_in_glioma_cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.100-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010046,"work_id":17906348,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039500,"email":"d***u@mail.cmu.edu.tw","display_order":0,"name":"Dah-yuu Lu","title":"Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells"},{"id":9010054,"work_id":17906348,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":4194304,"name":"Yuk-man Leung","title":"Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells"},{"id":9010111,"work_id":17906348,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039516,"email":"s***g@phys.sinica.edu.tw","display_order":6291456,"name":"Ssu-ming Huang","title":"Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma 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Migration","url":"https://www.academia.edu/Documents/in/Cell_Migration"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":60915,"name":"Cellular","url":"https://www.academia.edu/Documents/in/Cellular"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":76383,"name":"Glioma","url":"https://www.academia.edu/Documents/in/Glioma"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":1296969,"name":"Molecular and Cellular Biochemistry","url":"https://www.academia.edu/Documents/in/Molecular_and_Cellular_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2069878,"name":"Bradykinin","url":"https://www.academia.edu/Documents/in/Bradykinin"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906347"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906347/Phloroglucinol_derivative_MCPP_induces_cell_apoptosis_in_human_colon_cancer"><img alt="Research paper thumbnail of Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/42218619/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906347/Phloroglucinol_derivative_MCPP_induces_cell_apoptosis_in_human_colon_cancer">Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer</a></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">This study is the first to investigate the anticancer effects of the new phloroglucinol derivativ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2α (eIF-2α), suggesting the induction of ER stress. MCPP also increased GSK3α/β(Tyr270/216) phosphorylation and reduced GSK3α/β(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3α/β activation in mediating the MCPP-induced human colon cancer cell apoptosis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6df3aaa569125698c3e5e8d7dad559ad" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42218619,"asset_id":17906347,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42218619/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906347"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906347"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906347; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906347]").text(description); $(".js-view-count[data-work-id=17906347]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906347; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906347']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906347, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "6df3aaa569125698c3e5e8d7dad559ad" } } $('.js-work-strip[data-work-id=17906347]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906347,"title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer","translated_title":"","metadata":{"abstract":"This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2α (eIF-2α), suggesting the induction of ER stress. MCPP also increased GSK3α/β(Tyr270/216) phosphorylation and reduced GSK3α/β(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3α/β activation in mediating the MCPP-induced human colon cancer cell apoptosis.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Journal of Cellular Biochemistry"},"translated_abstract":"This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2α (eIF-2α), suggesting the induction of ER stress. MCPP also increased GSK3α/β(Tyr270/216) phosphorylation and reduced GSK3α/β(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3α/β activation in mediating the MCPP-induced human colon cancer cell apoptosis.","internal_url":"https://www.academia.edu/17906347/Phloroglucinol_derivative_MCPP_induces_cell_apoptosis_in_human_colon_cancer","translated_internal_url":"","created_at":"2015-11-07T06:50:11.003-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010029,"work_id":17906347,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2011212,"email":"y***n@mail.cmu.edu.tw","display_order":0,"name":"Yu-hsin Lin","title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer"},{"id":9010047,"work_id":17906347,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039500,"email":"d***u@mail.cmu.edu.tw","display_order":4194304,"name":"Dah-yuu Lu","title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer"},{"id":9010089,"work_id":17906347,"tagging_user_id":37822776,"tagged_user_id":38511809,"co_author_invite_id":2039505,"email":"c***g@mail.cmu.edu.tw","display_order":6291456,"name":"Chih-hsin Tang","title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer"},{"id":9010112,"work_id":17906347,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039516,"email":"s***g@phys.sinica.edu.tw","display_order":7340032,"name":"Ssu-ming Huang","title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer"},{"id":9010113,"work_id":17906347,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039517,"email":"c***g@ncree.narl.org.tw","display_order":7864320,"name":"Chih-shiang Chang","title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer"},{"id":9010120,"work_id":17906347,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039522,"email":"c***n@twna.org.tw","display_order":8126464,"name":"Jia-hong Chen","title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer"}],"downloadable_attachments":[{"id":42218619,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/42218619/thumbnails/1.jpg","file_name":"jcb.22966.pdf20160206-1436-piqjjl","download_url":"https://www.academia.edu/attachments/42218619/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Phloroglucinol_derivative_MCPP_induces_c.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/42218619/jcb.22966-libre.pdf20160206-1436-piqjjl?1454780620=\u0026response-content-disposition=attachment%3B+filename%3DPhloroglucinol_derivative_MCPP_induces_c.pdf\u0026Expires=1732348020\u0026Signature=N8RgAVoYv-6qKogo3BwF9QQlXJOX-P6~KfM-A-WQnqK5pTaHc411wTpbxsxxLQgxD~FbBGElYzrPbMuUkp2nXmv5KMKjmfo4jGpwU4tOOqoOF12llYOTrK6VD01uZaLPGwOUMMjOZsrm3UsALAH4uCexvFtvUqcU4Au8hQ3y0Mz3TU6wLwzjkGjlvd0rFALSxQFKSbd29dVnsob0zbOkFUtk7kGG2qJNHapBIMe03Z4Qx77fXiPpDckDM42M0n3X6DPVZWqhOOT61CFF81iX4-Tr8cHEjkJIRyWpmJSN~m2SGOlrz~3zon9KzIzU1135DeqdRNB3be9cE3rPB0CZzA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Phloroglucinol_derivative_MCPP_induces_cell_apoptosis_in_human_colon_cancer","translated_slug":"","page_count":10,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906346"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906346/Tetramethylpyrazine_protects_mice_against_thioacetamide_induced_acute_hepatotoxicity"><img alt="Research paper thumbnail of Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906346/Tetramethylpyrazine_protects_mice_against_thioacetamide_induced_acute_hepatotoxicity">Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a></span></div><div class="wp-workCard_item"><span>Journal of Biomedical Science</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatot...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. TMP appears to act by preventing lipid peroxidation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906346"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906346"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906346; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906346]").text(description); $(".js-view-count[data-work-id=17906346]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906346; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906346']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906346, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906346]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906346,"title":"Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity","translated_title":"","metadata":{"abstract":"In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. TMP appears to act by preventing lipid peroxidation.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Journal of Biomedical Science"},"translated_abstract":"In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. TMP appears to act by preventing lipid peroxidation.","internal_url":"https://www.academia.edu/17906346/Tetramethylpyrazine_protects_mice_against_thioacetamide_induced_acute_hepatotoxicity","translated_internal_url":"","created_at":"2015-11-07T06:50:10.904-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010027,"work_id":17906346,"tagging_user_id":37822776,"tagged_user_id":37925459,"co_author_invite_id":1975987,"email":"e***w@gmail.com","affiliation":"China Medical University,Taiwan","display_order":0,"name":"Edmund So","title":"Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity"},{"id":9010109,"work_id":17906346,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039515,"email":"c***6@uiuc.edu","display_order":4194304,"name":"Chi-feng Liu","title":"Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity"}],"downloadable_attachments":[],"slug":"Tetramethylpyrazine_protects_mice_against_thioacetamide_induced_acute_hepatotoxicity","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":36237,"name":"Biomedical","url":"https://www.academia.edu/Documents/in/Biomedical"},{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":77331,"name":"Biomedical science","url":"https://www.academia.edu/Documents/in/Biomedical_science"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":233372,"name":"Lipid peroxidation","url":"https://www.academia.edu/Documents/in/Lipid_peroxidation"},{"id":246560,"name":"High Pressure Liquid Chromatography","url":"https://www.academia.edu/Documents/in/High_Pressure_Liquid_Chromatography"},{"id":892147,"name":"Thioacetamide","url":"https://www.academia.edu/Documents/in/Thioacetamide"},{"id":1224429,"name":"Drug Induced Liver Injury","url":"https://www.academia.edu/Documents/in/Drug_Induced_Liver_Injury"},{"id":1281378,"name":"Aspartate Aminotransferases","url":"https://www.academia.edu/Documents/in/Aspartate_Aminotransferases"},{"id":1446339,"name":"Malondialdehyde","url":"https://www.academia.edu/Documents/in/Malondialdehyde"},{"id":1924712,"name":"Interleukin","url":"https://www.academia.edu/Documents/in/Interleukin"},{"id":2112739,"name":"Alanine Transaminase","url":"https://www.academia.edu/Documents/in/Alanine_Transaminase"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> </div><div class="profile--tab_content_container js-tab-pane tab-pane" data-section-id="3951676" id="papers"><div class="js-work-strip profile--work_container" data-work-id="17906364"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906364/Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model"><img alt="Research paper thumbnail of Preventive Treatment with Ketamine Attenuates the Ischaemia-Reperfusion Response in a Chronic Postischaemia Pain Model" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906364/Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model">Preventive Treatment with Ketamine Attenuates the Ischaemia-Reperfusion Response in a Chronic Postischaemia Pain Model</a></div><div class="wp-workCard_item"><span>Oxidative Medicine and Cellular Longevity</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome (CRPS). Ketamine has proposed anti-inflammatory effects and has been used for treating CRPS. This study aimed to evaluate anti-inflammatory and analgesic effects of ketamine after ischaemia-reperfusion injury in a chronic postischaemia pain (CPIP) model of CRPS-I. Using this model, ischemia was induced in the hindlimbs of male Sprague-Dawley rats. Ketamine, methylprednisolone, or saline was administered immediately after reperfusion. Physical effects, (oedema, temperature, and mechanical and cold allodynia) in the bilateral hindpaws, were assessed from 48 hours after reperfusion. Fewer (56%) rats in the ketamine group developed CPIP at the 48th hour after reperfusion (nonsignificant). Ketamine treated rats showed a significantly lower temperature in the ischaemic hindpaw compared to saline (P &amp;amp;amp;amp;amp;amp;amp;lt; 0.01) and methylprednisolone (P &amp;amp;amp;amp;amp;amp;amp;lt; 0.05) groups. Mechanical and cold allodynia were significantly lower in the ischaemic side in the ketamine group (P &amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Proinflammatory cytokines TNF-α and IL-2 were significantly lower at the 48th hour after reperfusion in ketamine and methylprednisolone groups, compared to saline (all P &amp;amp;amp;amp;amp;amp;amp;lt; 0.05). In conclusion, immediate administration of ketamine after an ischaemia-reperfusion injury can alleviate pain and inflammation in the CPIP model and has potential to treat postischaemic pain.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906364"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906364"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906364; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906364]").text(description); $(".js-view-count[data-work-id=17906364]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906364; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906364']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906364, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906364]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906364,"title":"Preventive Treatment with Ketamine Attenuates the Ischaemia-Reperfusion Response in a Chronic Postischaemia Pain Model","translated_title":"","metadata":{"abstract":"Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome (CRPS). Ketamine has proposed anti-inflammatory effects and has been used for treating CRPS. This study aimed to evaluate anti-inflammatory and analgesic effects of ketamine after ischaemia-reperfusion injury in a chronic postischaemia pain (CPIP) model of CRPS-I. Using this model, ischemia was induced in the hindlimbs of male Sprague-Dawley rats. Ketamine, methylprednisolone, or saline was administered immediately after reperfusion. Physical effects, (oedema, temperature, and mechanical and cold allodynia) in the bilateral hindpaws, were assessed from 48 hours after reperfusion. Fewer (56%) rats in the ketamine group developed CPIP at the 48th hour after reperfusion (nonsignificant). Ketamine treated rats showed a significantly lower temperature in the ischaemic hindpaw compared to saline (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.01) and methylprednisolone (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05) groups. Mechanical and cold allodynia were significantly lower in the ischaemic side in the ketamine group (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Proinflammatory cytokines TNF-α and IL-2 were significantly lower at the 48th hour after reperfusion in ketamine and methylprednisolone groups, compared to saline (all P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). In conclusion, immediate administration of ketamine after an ischaemia-reperfusion injury can alleviate pain and inflammation in the CPIP model and has potential to treat postischaemic pain.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"Oxidative Medicine and Cellular Longevity"},"translated_abstract":"Ischemia and inflammation may be pathophysiological mechanisms of complex regional pain syndrome (CRPS). Ketamine has proposed anti-inflammatory effects and has been used for treating CRPS. This study aimed to evaluate anti-inflammatory and analgesic effects of ketamine after ischaemia-reperfusion injury in a chronic postischaemia pain (CPIP) model of CRPS-I. Using this model, ischemia was induced in the hindlimbs of male Sprague-Dawley rats. Ketamine, methylprednisolone, or saline was administered immediately after reperfusion. Physical effects, (oedema, temperature, and mechanical and cold allodynia) in the bilateral hindpaws, were assessed from 48 hours after reperfusion. Fewer (56%) rats in the ketamine group developed CPIP at the 48th hour after reperfusion (nonsignificant). Ketamine treated rats showed a significantly lower temperature in the ischaemic hindpaw compared to saline (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.01) and methylprednisolone (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05) groups. Mechanical and cold allodynia were significantly lower in the ischaemic side in the ketamine group (P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). Proinflammatory cytokines TNF-α and IL-2 were significantly lower at the 48th hour after reperfusion in ketamine and methylprednisolone groups, compared to saline (all P \u0026amp;amp;amp;amp;amp;amp;amp;lt; 0.05). In conclusion, immediate administration of ketamine after an ischaemia-reperfusion injury can alleviate pain and inflammation in the CPIP model and has potential to treat postischaemic pain.","internal_url":"https://www.academia.edu/17906364/Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model","translated_internal_url":"","created_at":"2015-11-07T06:50:12.594-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Preventive_Treatment_with_Ketamine_Attenuates_the_Ischaemia_Reperfusion_Response_in_a_Chronic_Postischaemia_Pain_Model","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906363"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906363/Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells"><img alt="Research paper thumbnail of Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906363/Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells">Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells</a></div><div class="wp-workCard_item"><span>European Journal of Pharmacology</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) con...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) concentration ([Ca(2+)]i) and is of prime importance in vascular tone regulation as NO relaxes vascular smooth muscle. Agonists could stimulate EC [Ca(2+)]i elevation by triggering Ca(2+) influx via plasma membrane ion channels, one of which is the store-operated Ca(2+) channel; the latter opens as a result of agonist-triggered internal Ca(2+) release. Endotoxin (lipopolysaccharide, LPS) could cause sepsis, which is often the fatal cause in critically ill patients. One of the LPS-induced damages is EC dysfunction, eventually leading to perturbations in hemodynamics. We obtained data showing that LPS-challenged mouse cerebral cortex endothelial bEND.3 cells did not suffer from apoptotic death, and in fact had intact agonist-triggered intracellular Ca(2+) release; however, they had reduced store-operated Ca(2+) entry (SOCE) after LPS treatment for 3h or more. Using real-time PCR, we did not find a decrease in gene expression of stromal interaction molecule 1 (STIM1) and Orai1 (two SOCE protein components) in bEND.3 cells treated with LPS for 15h. LPS inhibitory effects could be largely prevented by sodium salicylate (an inhibitor of nuclear factor-κB; NF-κB) or SB203580 (an inhibitor of p38 mitogen-activated protein kinases; p38 MAPK), suggesting that the p38 MAPK-NF-κB pathway is involved in SOCE inhibition.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906363"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906363"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906363; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906363]").text(description); $(".js-view-count[data-work-id=17906363]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906363; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906363']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906363, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906363]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906363,"title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells","translated_title":"","metadata":{"abstract":"Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) concentration ([Ca(2+)]i) and is of prime importance in vascular tone regulation as NO relaxes vascular smooth muscle. Agonists could stimulate EC [Ca(2+)]i elevation by triggering Ca(2+) influx via plasma membrane ion channels, one of which is the store-operated Ca(2+) channel; the latter opens as a result of agonist-triggered internal Ca(2+) release. Endotoxin (lipopolysaccharide, LPS) could cause sepsis, which is often the fatal cause in critically ill patients. One of the LPS-induced damages is EC dysfunction, eventually leading to perturbations in hemodynamics. We obtained data showing that LPS-challenged mouse cerebral cortex endothelial bEND.3 cells did not suffer from apoptotic death, and in fact had intact agonist-triggered intracellular Ca(2+) release; however, they had reduced store-operated Ca(2+) entry (SOCE) after LPS treatment for 3h or more. Using real-time PCR, we did not find a decrease in gene expression of stromal interaction molecule 1 (STIM1) and Orai1 (two SOCE protein components) in bEND.3 cells treated with LPS for 15h. LPS inhibitory effects could be largely prevented by sodium salicylate (an inhibitor of nuclear factor-κB; NF-κB) or SB203580 (an inhibitor of p38 mitogen-activated protein kinases; p38 MAPK), suggesting that the p38 MAPK-NF-κB pathway is involved in SOCE inhibition.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"European Journal of Pharmacology"},"translated_abstract":"Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) concentration ([Ca(2+)]i) and is of prime importance in vascular tone regulation as NO relaxes vascular smooth muscle. Agonists could stimulate EC [Ca(2+)]i elevation by triggering Ca(2+) influx via plasma membrane ion channels, one of which is the store-operated Ca(2+) channel; the latter opens as a result of agonist-triggered internal Ca(2+) release. Endotoxin (lipopolysaccharide, LPS) could cause sepsis, which is often the fatal cause in critically ill patients. One of the LPS-induced damages is EC dysfunction, eventually leading to perturbations in hemodynamics. We obtained data showing that LPS-challenged mouse cerebral cortex endothelial bEND.3 cells did not suffer from apoptotic death, and in fact had intact agonist-triggered intracellular Ca(2+) release; however, they had reduced store-operated Ca(2+) entry (SOCE) after LPS treatment for 3h or more. Using real-time PCR, we did not find a decrease in gene expression of stromal interaction molecule 1 (STIM1) and Orai1 (two SOCE protein components) in bEND.3 cells treated with LPS for 15h. LPS inhibitory effects could be largely prevented by sodium salicylate (an inhibitor of nuclear factor-κB; NF-κB) or SB203580 (an inhibitor of p38 mitogen-activated protein kinases; p38 MAPK), suggesting that the p38 MAPK-NF-κB pathway is involved in SOCE inhibition.","internal_url":"https://www.academia.edu/17906363/Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells","translated_internal_url":"","created_at":"2015-11-07T06:50:12.524-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010052,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":9493235,"co_author_invite_id":null,"email":"a***2@gmail.com","display_order":0,"name":"Tzu-hui su","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010060,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":4194304,"name":"Yuk-man Leung","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010078,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039504,"email":"m***g@mail.tku.edu.tw","display_order":6291456,"name":"Mei-ling Wang","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010088,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010099,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039509,"email":"z***u@sina.com.cn","display_order":7864320,"name":"Zhong-min Liu","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010100,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039510,"email":"l***u@cycu.edu.tw","display_order":8126464,"name":"Shyh-liang Lou","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"},{"id":9010114,"work_id":17906363,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039518,"email":"t***0@gmail.com","display_order":8257536,"name":"Tien-yao Tsai","title":"Suppression of Ca2+ influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells"}],"downloadable_attachments":[],"slug":"Suppression_of_Ca2_influx_in_endotoxin_treated_mouse_cerebral_cortex_endothelial_bEND_3_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906361"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906361/Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes"><img alt="Research paper thumbnail of Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906361/Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes">Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes</a></div><div class="wp-workCard_item"><span>Pharmacological Reports</span><span>, 2014</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also play an active role in modulating synaptic transmission. Palmitic acid (PA) is a saturated fatty acid which, when being excessive, is a significant risk factor for lipotoxicity. Activation of astrocytes by PA has been shown to cause neuronal inflammation and demyelination. However, direct damage by PA to astrocytes is relatively unexplored. The aim of this study was to identify the mechanism(s) of PA-induced cytotoxicity in rat cortical astrocytes and possible protection by (+)-catechin. Cytotoxicity and endoplasmic reticulum (ER) markers were assessed by MTT assay and Western blotting, respectively. Cytosolic Ca(2+) and mitochondrial membrane potential (MMP) were measured microfluorimetrically using fura-2 and rhodamine 123, respectively. Intracellular reactive oxygen species (ROS) production was assayed by the indicator 2&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-7&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorodihydrofluorescein diacetate. Exposure of astrocytes to 100μM PA for 24h resulted in apoptotic cell death. Whilst PA-induced cell death appeared to be unrelated to ER stress and perturbation in cytosolic Ca(2+) signaling, it was likely a result of ROS production and subsequent MMP collapse, since ascorbic acid (anti-oxidant, 100μM) prevented PA-induced MMP collapse and cell death. Co-treatment of astrocytes with (+)-catechin (300μM), an anti-oxidant found abundantly in green tea, significantly prevented PA-induced ROS production, MMP collapse and cell death. Our results suggest that PA-induced cytotoxicity in astrocytes may involve ROS generation and MMP collapse, which can be prevented by (+)-catechin.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906361"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906361"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906361; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906361]").text(description); $(".js-view-count[data-work-id=17906361]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906361; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906361']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906361, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906361]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906361,"title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes","translated_title":"","metadata":{"abstract":"Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also play an active role in modulating synaptic transmission. Palmitic acid (PA) is a saturated fatty acid which, when being excessive, is a significant risk factor for lipotoxicity. Activation of astrocytes by PA has been shown to cause neuronal inflammation and demyelination. However, direct damage by PA to astrocytes is relatively unexplored. The aim of this study was to identify the mechanism(s) of PA-induced cytotoxicity in rat cortical astrocytes and possible protection by (+)-catechin. Cytotoxicity and endoplasmic reticulum (ER) markers were assessed by MTT assay and Western blotting, respectively. Cytosolic Ca(2+) and mitochondrial membrane potential (MMP) were measured microfluorimetrically using fura-2 and rhodamine 123, respectively. Intracellular reactive oxygen species (ROS) production was assayed by the indicator 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorodihydrofluorescein diacetate. Exposure of astrocytes to 100μM PA for 24h resulted in apoptotic cell death. Whilst PA-induced cell death appeared to be unrelated to ER stress and perturbation in cytosolic Ca(2+) signaling, it was likely a result of ROS production and subsequent MMP collapse, since ascorbic acid (anti-oxidant, 100μM) prevented PA-induced MMP collapse and cell death. Co-treatment of astrocytes with (+)-catechin (300μM), an anti-oxidant found abundantly in green tea, significantly prevented PA-induced ROS production, MMP collapse and cell death. Our results suggest that PA-induced cytotoxicity in astrocytes may involve ROS generation and MMP collapse, which can be prevented by (+)-catechin.","publication_date":{"day":null,"month":null,"year":2014,"errors":{}},"publication_name":"Pharmacological Reports"},"translated_abstract":"Astrocytes do not only maintain homeostasis of the extracellular milieu of the neurons, but also play an active role in modulating synaptic transmission. Palmitic acid (PA) is a saturated fatty acid which, when being excessive, is a significant risk factor for lipotoxicity. Activation of astrocytes by PA has been shown to cause neuronal inflammation and demyelination. However, direct damage by PA to astrocytes is relatively unexplored. The aim of this study was to identify the mechanism(s) of PA-induced cytotoxicity in rat cortical astrocytes and possible protection by (+)-catechin. Cytotoxicity and endoplasmic reticulum (ER) markers were assessed by MTT assay and Western blotting, respectively. Cytosolic Ca(2+) and mitochondrial membrane potential (MMP) were measured microfluorimetrically using fura-2 and rhodamine 123, respectively. Intracellular reactive oxygen species (ROS) production was assayed by the indicator 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorodihydrofluorescein diacetate. Exposure of astrocytes to 100μM PA for 24h resulted in apoptotic cell death. Whilst PA-induced cell death appeared to be unrelated to ER stress and perturbation in cytosolic Ca(2+) signaling, it was likely a result of ROS production and subsequent MMP collapse, since ascorbic acid (anti-oxidant, 100μM) prevented PA-induced MMP collapse and cell death. Co-treatment of astrocytes with (+)-catechin (300μM), an anti-oxidant found abundantly in green tea, significantly prevented PA-induced ROS production, MMP collapse and cell death. Our results suggest that PA-induced cytotoxicity in astrocytes may involve ROS generation and MMP collapse, which can be prevented by (+)-catechin.","internal_url":"https://www.academia.edu/17906361/Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes","translated_internal_url":"","created_at":"2015-11-07T06:50:12.350-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010045,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039500,"email":"d***u@mail.cmu.edu.tw","display_order":0,"name":"Dah-yuu Lu","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010051,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":9493235,"co_author_invite_id":null,"email":"a***2@gmail.com","display_order":4194304,"name":"Tzu-hui su","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010053,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":6291456,"name":"Yuk-man Leung","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010082,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010098,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039509,"email":"z***u@sina.com.cn","display_order":7864320,"name":"Zhong-min Liu","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010124,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039524,"email":"k***g@mail.cmu.edu.tw","display_order":8126464,"name":"Ka-shun Cheng","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"},{"id":9010132,"work_id":17906361,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039530,"email":"y***u@ms2.mmh.org.tw","display_order":8257536,"name":"Yu-ru Wu","title":"Palmitic acid-induced lipotoxicity and protection by (+)-catechin in rat cortical astrocytes"}],"downloadable_attachments":[],"slug":"Palmitic_acid_induced_lipotoxicity_and_protection_by_catechin_in_rat_cortical_astrocytes","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":9534,"name":"Calcium","url":"https://www.academia.edu/Documents/in/Calcium"},{"id":18459,"name":"Endoplasmic Reticulum Stress","url":"https://www.academia.edu/Documents/in/Endoplasmic_Reticulum_Stress"},{"id":24731,"name":"Apoptosis","url":"https://www.academia.edu/Documents/in/Apoptosis"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":78467,"name":"Cerebral Cortex","url":"https://www.academia.edu/Documents/in/Cerebral_Cortex"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":196442,"name":"Astrocytes","url":"https://www.academia.edu/Documents/in/Astrocytes"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":1223957,"name":"Catechin","url":"https://www.academia.edu/Documents/in/Catechin"},{"id":1260596,"name":"Palmitic Acid","url":"https://www.academia.edu/Documents/in/Palmitic_Acid"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906360"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906360/Tetramethylpyrazine_Inhibits_Angiotensin_II_Increased_NAD_P_H_Oxidase_Activity_and_Subsequent_Proliferation_in_Rat_Aortic_Smooth_Muscle_Cells"><img alt="Research paper thumbnail of Tetramethylpyrazine Inhibits Angiotensin II-Increased NAD(P)H Oxidase Activity and Subsequent Proliferation in Rat Aortic Smooth Muscle Cells" class="work-thumbnail" src="https://attachments.academia-assets.com/39773305/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906360/Tetramethylpyrazine_Inhibits_Angiotensin_II_Increased_NAD_P_H_Oxidase_Activity_and_Subsequent_Proliferation_in_Rat_Aortic_Smooth_Muscle_Cells">Tetramethylpyrazine Inhibits Angiotensin II-Increased NAD(P)H Oxidase Activity and Subsequent Proliferation in Rat Aortic Smooth Muscle Cells</a></div><div class="wp-workCard_item"><span>The American Journal of Chinese Medicine</span><span>, 2007</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="d16b3e949280e4d2457fd1af08e033b0" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773305,"asset_id":17906360,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773305/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&st=MTczMjM3NDc1OCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906360"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906360"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906360; 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The aims of this study were to examine whether TMP may alter angiotenisn II (Ang II)-induced proliferation and to identify the putative underlying signaling pathways in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with TMP and then stimulated with Ang II, [ 3 H]-thymidine incorporation and the ET-1 expression was examined. Ang II increased DNA synthesis which was inhibited by TMP (1-100 µM). TMP inhibited the Ang II-induced ET-1 mRNA levels and ET-1 secretion. TMP also inhibited Ang II-increased NAD(P)H oxidase activity, intracellular reactive oxygen species (ROS) levels, and the ERK phosphorylation. Furthermore, TMP and antioxidants such as Trolox and diphenylene iodonium decreased Ang II-induced ERK phosphorylation, and activator protein-1 reporter activity. In summary, we demonstrate for the first time that TMP inhibits Ang II-induced proliferation and ET-1, partially by interfering with the ERK pathway via attenuation of Ang II-increased NAD(P)H oxidase and ROS generation. 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class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906359/Isosteviol_as_a_Potassium_Channel_Opener_to_Lower_Intracellular_Calcium_Concentrations_in_Cultured_Aortic_Smooth_Muscle_Cells">Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/TzhurngCheng">Tz-hurng Cheng</a></span></div><div class="wp-workCard_item"><span>Planta Medica</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly use...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly used as a non-caloric sugar substitute in Japan and Brazil. The present study attempted to elucidate the role of potassium (K (+)) channels in the action of isosteviol on intracellular calcium concentrations ([Ca (2+)]i) in cultured vascular smooth muscle (A7r5) cells using the Ca (2+)-sensitive dye Fura-2 as an indicator. The increase of [Ca (2+)]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by isosteviol from 0.01 micromol/L to 10 micromol/L. The attenuation by isosteviol of the vasopressin- and phenylephrine-induced increase in [Ca (2+)]i was inhibited by glibenclamide, apamin and 4-aminopyridine but not by charybdotoxin. Furthermore, the inhibitory action of isosteviol on [Ca (2+)]i was blocked when A7r5 cells co-treated with glibenclamide and apamin in conjunction with 4-aminopyridine were present. Therefore, not only did the ATP-sensitive potassium (K (ATP)) channel affect the action of isosteviol on [Ca (2+)]i modulation in A7r5 cells, but also those on the small conductance calcium-activated potassium (SK (Ca)) channels and voltage-gated (Kv) channels. However, the blockers of large-conductance Ca (2+)-activated potassium channels failed to modify the inhibitory action of isosteviol on [Ca (2+)]i. The obtained results indicated that a decrease of [Ca (2+)]i in A7r5 cells by isosteviol is mainly mediated by the selective opening of K (ATP) channel or/and SK (Ca) channel. Alteration in the Kv channel also plays a critical role in the inhibitory action of isosteviol.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906359"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906359"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906359; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906359]").text(description); $(".js-view-count[data-work-id=17906359]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906359; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906359']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906359, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906359]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906359,"title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells","translated_title":"","metadata":{"abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly used as a non-caloric sugar substitute in Japan and Brazil. The present study attempted to elucidate the role of potassium (K (+)) channels in the action of isosteviol on intracellular calcium concentrations ([Ca (2+)]i) in cultured vascular smooth muscle (A7r5) cells using the Ca (2+)-sensitive dye Fura-2 as an indicator. The increase of [Ca (2+)]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by isosteviol from 0.01 micromol/L to 10 micromol/L. The attenuation by isosteviol of the vasopressin- and phenylephrine-induced increase in [Ca (2+)]i was inhibited by glibenclamide, apamin and 4-aminopyridine but not by charybdotoxin. Furthermore, the inhibitory action of isosteviol on [Ca (2+)]i was blocked when A7r5 cells co-treated with glibenclamide and apamin in conjunction with 4-aminopyridine were present. Therefore, not only did the ATP-sensitive potassium (K (ATP)) channel affect the action of isosteviol on [Ca (2+)]i modulation in A7r5 cells, but also those on the small conductance calcium-activated potassium (SK (Ca)) channels and voltage-gated (Kv) channels. However, the blockers of large-conductance Ca (2+)-activated potassium channels failed to modify the inhibitory action of isosteviol on [Ca (2+)]i. The obtained results indicated that a decrease of [Ca (2+)]i in A7r5 cells by isosteviol is mainly mediated by the selective opening of K (ATP) channel or/and SK (Ca) channel. Alteration in the Kv channel also plays a critical role in the inhibitory action of isosteviol.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Planta Medica"},"translated_abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, and is commonly used as a non-caloric sugar substitute in Japan and Brazil. The present study attempted to elucidate the role of potassium (K (+)) channels in the action of isosteviol on intracellular calcium concentrations ([Ca (2+)]i) in cultured vascular smooth muscle (A7r5) cells using the Ca (2+)-sensitive dye Fura-2 as an indicator. The increase of [Ca (2+)]i in A7r5 cells produced by vasopressin (1 micromol/L) or phenylephrine (1 micromol/L) was attenuated by isosteviol from 0.01 micromol/L to 10 micromol/L. The attenuation by isosteviol of the vasopressin- and phenylephrine-induced increase in [Ca (2+)]i was inhibited by glibenclamide, apamin and 4-aminopyridine but not by charybdotoxin. Furthermore, the inhibitory action of isosteviol on [Ca (2+)]i was blocked when A7r5 cells co-treated with glibenclamide and apamin in conjunction with 4-aminopyridine were present. Therefore, not only did the ATP-sensitive potassium (K (ATP)) channel affect the action of isosteviol on [Ca (2+)]i modulation in A7r5 cells, but also those on the small conductance calcium-activated potassium (SK (Ca)) channels and voltage-gated (Kv) channels. However, the blockers of large-conductance Ca (2+)-activated potassium channels failed to modify the inhibitory action of isosteviol on [Ca (2+)]i. The obtained results indicated that a decrease of [Ca (2+)]i in A7r5 cells by isosteviol is mainly mediated by the selective opening of K (ATP) channel or/and SK (Ca) channel. Alteration in the Kv channel also plays a critical role in the inhibitory action of isosteviol.","internal_url":"https://www.academia.edu/17906359/Isosteviol_as_a_Potassium_Channel_Opener_to_Lower_Intracellular_Calcium_Concentrations_in_Cultured_Aortic_Smooth_Muscle_Cells","translated_internal_url":"","created_at":"2015-11-07T06:50:12.171-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010039,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":118320,"email":"e***m@hindawi.com","display_order":0,"name":"I-min Liu","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010044,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":4194304,"name":"Juei-tang Cheng","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010067,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":37939559,"co_author_invite_id":836505,"email":"h***0@tmu.edu.tw","display_order":6291456,"name":"H.-h. Hsu","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010087,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"},{"id":9010128,"work_id":17906359,"tagging_user_id":37822776,"tagged_user_id":39564542,"co_author_invite_id":2039526,"email":"t***g@gate.sinica.edu.tw","display_order":7864320,"name":"Tz-hurng Cheng","title":"Isosteviol as a Potassium Channel Opener to Lower Intracellular Calcium Concentrations in Cultured Aortic Smooth Muscle Cells"}],"downloadable_attachments":[],"slug":"Isosteviol_as_a_Potassium_Channel_Opener_to_Lower_Intracellular_Calcium_Concentrations_in_Cultured_Aortic_Smooth_Muscle_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4083,"name":"Complementary and Alternative Medicine","url":"https://www.academia.edu/Documents/in/Complementary_and_Alternative_Medicine"},{"id":5541,"name":"Plant Biology","url":"https://www.academia.edu/Documents/in/Plant_Biology"},{"id":9534,"name":"Calcium","url":"https://www.academia.edu/Documents/in/Calcium"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":57808,"name":"Cell line","url":"https://www.academia.edu/Documents/in/Cell_line"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":416452,"name":"Diterpenes","url":"https://www.academia.edu/Documents/in/Diterpenes"},{"id":521072,"name":"Stevia","url":"https://www.academia.edu/Documents/in/Stevia"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1134083,"name":"Medicinal Plant","url":"https://www.academia.edu/Documents/in/Medicinal_Plant"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906358"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906358/Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension"><img alt="Research paper thumbnail of Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906358/Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension">Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension</a></div><div class="wp-workCard_item"><span>Planta Medica</span><span>, 2001</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (Compositae). It has been used popularly in Japan and Brazil as a sugar substitute for decades. Previous study has shown that it lowered blood pressure in spontaneously hypertensive rats (SHRs) when administered intravenously. This study shows that intraperitoneal injection of stevioside 25 mg/kg also has antihypertensive effect in SHRs. In isolated aortic rings from normal rats, stevioside could dose-dependently relax the vasopressin-induced vasoconstriction in both the presence and absence of endothelium. However, stevioside had no effect on phenylephrine- and KCl-induced phasic vasoconstriction. In addition, stevioside lost its influence on vasopressin-induced vasoconstriction in Ca(2+)-free medium. The results indicate that stevioside caused vasorelaxation via an inhibition of Ca(2+) influx into the blood vessel. This phenomenon was further confirmed in cultured aortic smooth muscle cells (A7r5). Using 10(-5) M methylene blue for 15 min, stevioside could still relax 10(-8) M vasopressin-induced vasoconstriction in isolated rat aortic rings, showing that this vasorelaxation effect was not related to nitric oxide. The present data show that the vasorelexation effect of stevioside was mediated mainly through Ca(2+) influx inhibition.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906358"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906358"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906358; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906358]").text(description); $(".js-view-count[data-work-id=17906358]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906358; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906358']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906358, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906358]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906358,"title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension","translated_title":"","metadata":{"abstract":"Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (Compositae). It has been used popularly in Japan and Brazil as a sugar substitute for decades. Previous study has shown that it lowered blood pressure in spontaneously hypertensive rats (SHRs) when administered intravenously. This study shows that intraperitoneal injection of stevioside 25 mg/kg also has antihypertensive effect in SHRs. In isolated aortic rings from normal rats, stevioside could dose-dependently relax the vasopressin-induced vasoconstriction in both the presence and absence of endothelium. However, stevioside had no effect on phenylephrine- and KCl-induced phasic vasoconstriction. In addition, stevioside lost its influence on vasopressin-induced vasoconstriction in Ca(2+)-free medium. The results indicate that stevioside caused vasorelaxation via an inhibition of Ca(2+) influx into the blood vessel. This phenomenon was further confirmed in cultured aortic smooth muscle cells (A7r5). Using 10(-5) M methylene blue for 15 min, stevioside could still relax 10(-8) M vasopressin-induced vasoconstriction in isolated rat aortic rings, showing that this vasorelaxation effect was not related to nitric oxide. The present data show that the vasorelexation effect of stevioside was mediated mainly through Ca(2+) influx inhibition.","publication_date":{"day":null,"month":null,"year":2001,"errors":{}},"publication_name":"Planta Medica"},"translated_abstract":"Stevioside is a sweet-tasting glycoside occurring abundantly in the leaves of Stevia rebaudiana (Compositae). It has been used popularly in Japan and Brazil as a sugar substitute for decades. Previous study has shown that it lowered blood pressure in spontaneously hypertensive rats (SHRs) when administered intravenously. This study shows that intraperitoneal injection of stevioside 25 mg/kg also has antihypertensive effect in SHRs. In isolated aortic rings from normal rats, stevioside could dose-dependently relax the vasopressin-induced vasoconstriction in both the presence and absence of endothelium. However, stevioside had no effect on phenylephrine- and KCl-induced phasic vasoconstriction. In addition, stevioside lost its influence on vasopressin-induced vasoconstriction in Ca(2+)-free medium. The results indicate that stevioside caused vasorelaxation via an inhibition of Ca(2+) influx into the blood vessel. This phenomenon was further confirmed in cultured aortic smooth muscle cells (A7r5). Using 10(-5) M methylene blue for 15 min, stevioside could still relax 10(-8) M vasopressin-induced vasoconstriction in isolated rat aortic rings, showing that this vasorelaxation effect was not related to nitric oxide. The present data show that the vasorelexation effect of stevioside was mediated mainly through Ca(2+) influx inhibition.","internal_url":"https://www.academia.edu/17906358/Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension","translated_internal_url":"","created_at":"2015-11-07T06:50:12.084-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010041,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":0,"name":"Juei-tang Cheng","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"},{"id":9010083,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":4194304,"name":"Paul Chan","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"},{"id":9010097,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":38571549,"co_author_invite_id":414721,"email":"y***n@coh.org","display_order":6291456,"name":"Yi-jen Chen","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"},{"id":9010127,"work_id":17906358,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":711477,"email":"l***6@knjc.edu.tw","display_order":7340032,"name":"Chun-nin Lee","title":"Inhibitory Effect of Stevioside on Calcium Influx to Produce Antihypertension"}],"downloadable_attachments":[],"slug":"Inhibitory_Effect_of_Stevioside_on_Calcium_Influx_to_Produce_Antihypertension","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4083,"name":"Complementary and Alternative Medicine","url":"https://www.academia.edu/Documents/in/Complementary_and_Alternative_Medicine"},{"id":5541,"name":"Plant Biology","url":"https://www.academia.edu/Documents/in/Plant_Biology"},{"id":9534,"name":"Calcium","url":"https://www.academia.edu/Documents/in/Calcium"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":71399,"name":"Hypertension","url":"https://www.academia.edu/Documents/in/Hypertension"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":165799,"name":"Terpenes","url":"https://www.academia.edu/Documents/in/Terpenes"},{"id":194060,"name":"Asteraceae","url":"https://www.academia.edu/Documents/in/Asteraceae"},{"id":204388,"name":"Vasoconstriction","url":"https://www.academia.edu/Documents/in/Vasoconstriction"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":416452,"name":"Diterpenes","url":"https://www.academia.edu/Documents/in/Diterpenes"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1322750,"name":"Planta","url":"https://www.academia.edu/Documents/in/Planta"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906357"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906357/Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells"><img alt="Research paper thumbnail of Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906357/Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells">Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells</a></div><div class="wp-workCard_item"><span>Planta Medica</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective pro...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective properties. Not much is known about the effects of osthol on ionic channels, activities of which are implicated in vasorelaxation and neuroprotection. In this work we report that osthol could inhibit voltage-gated Na (+) currents with state-dependence in mouse neuroblastoma N2A cells (IC (50) = 12.3 microM and 31.5 microM at holding potentials of - 70 mV and - 100 mV, respectively). Current blockade was equally effective in both extracellular and intracellular application of osthol. Osthol (18 microM) did not significantly affect the kinetics and voltage-dependence of Na (+) channel activation, but left-shifted the steady-state inactivation curve (V (1/2) = - 60.5 mV and - 78.7 mV in the absence and presence of osthol, respectively). Osthol also mildly but significantly retarded channel recovery from inactivation (recovery time constant = 19.9 ms and 35.6 ms in the absence and presence of osthol, respectively). In addition, osthol blocked Na (+) currents in a frequency-dependent fashion: blockades of 17 %, 34 % and 49 % when currents were triggered at 0.33 Hz, 1 Hz and 3.33 Hz, respectively. Taken together, our results therefore suggest that osthol blocked voltage-gated Na (+) channels intracellularly with state- and frequency-dependence.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906357"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906357"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906357; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906357]").text(description); $(".js-view-count[data-work-id=17906357]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906357; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906357']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906357, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906357]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906357,"title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells","translated_title":"","metadata":{"abstract":"Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective properties. Not much is known about the effects of osthol on ionic channels, activities of which are implicated in vasorelaxation and neuroprotection. In this work we report that osthol could inhibit voltage-gated Na (+) currents with state-dependence in mouse neuroblastoma N2A cells (IC (50) = 12.3 microM and 31.5 microM at holding potentials of - 70 mV and - 100 mV, respectively). Current blockade was equally effective in both extracellular and intracellular application of osthol. Osthol (18 microM) did not significantly affect the kinetics and voltage-dependence of Na (+) channel activation, but left-shifted the steady-state inactivation curve (V (1/2) = - 60.5 mV and - 78.7 mV in the absence and presence of osthol, respectively). Osthol also mildly but significantly retarded channel recovery from inactivation (recovery time constant = 19.9 ms and 35.6 ms in the absence and presence of osthol, respectively). In addition, osthol blocked Na (+) currents in a frequency-dependent fashion: blockades of 17 %, 34 % and 49 % when currents were triggered at 0.33 Hz, 1 Hz and 3.33 Hz, respectively. Taken together, our results therefore suggest that osthol blocked voltage-gated Na (+) channels intracellularly with state- and frequency-dependence.","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"Planta Medica"},"translated_abstract":"Osthol, a Chinese herbal compound, has been shown to possess vasorelaxant and neuroprotective properties. Not much is known about the effects of osthol on ionic channels, activities of which are implicated in vasorelaxation and neuroprotection. In this work we report that osthol could inhibit voltage-gated Na (+) currents with state-dependence in mouse neuroblastoma N2A cells (IC (50) = 12.3 microM and 31.5 microM at holding potentials of - 70 mV and - 100 mV, respectively). Current blockade was equally effective in both extracellular and intracellular application of osthol. Osthol (18 microM) did not significantly affect the kinetics and voltage-dependence of Na (+) channel activation, but left-shifted the steady-state inactivation curve (V (1/2) = - 60.5 mV and - 78.7 mV in the absence and presence of osthol, respectively). Osthol also mildly but significantly retarded channel recovery from inactivation (recovery time constant = 19.9 ms and 35.6 ms in the absence and presence of osthol, respectively). In addition, osthol blocked Na (+) currents in a frequency-dependent fashion: blockades of 17 %, 34 % and 49 % when currents were triggered at 0.33 Hz, 1 Hz and 3.33 Hz, respectively. Taken together, our results therefore suggest that osthol blocked voltage-gated Na (+) channels intracellularly with state- and frequency-dependence.","internal_url":"https://www.academia.edu/17906357/Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.985-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010058,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":0,"name":"Yuk-man Leung","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010071,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":128927,"email":"k***h@mail.cmu.edu.tw","display_order":4194304,"name":"Yueh-hsiung Kuo","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010080,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":23641462,"co_author_invite_id":null,"email":"l***g@gmail.com","affiliation":"China Medical University,Taiwan","display_order":6291456,"name":"Li-Chi Chiang","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010096,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039508,"email":"u***7@cmu.edu.tw","display_order":7340032,"name":"Yi-huan Tsou","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010105,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039512,"email":"c***9@stsipa.gov.tw","display_order":7864320,"name":"Chun-hsiao Chou","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"},{"id":9010116,"work_id":17906357,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039519,"email":"c***o@twna.org.tw","display_order":8126464,"name":"Chia-chia Chao","title":"Osthol is a Use-Dependent Blocker of Voltage-Gated Na + Channels in Mouse Neuroblastoma N2A Cells"}],"downloadable_attachments":[],"slug":"Osthol_is_a_Use_Dependent_Blocker_of_Voltage_Gated_Na_Channels_in_Mouse_Neuroblastoma_N2A_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4083,"name":"Complementary and Alternative Medicine","url":"https://www.academia.edu/Documents/in/Complementary_and_Alternative_Medicine"},{"id":5541,"name":"Plant Biology","url":"https://www.academia.edu/Documents/in/Plant_Biology"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":256805,"name":"Neuroblastoma","url":"https://www.academia.edu/Documents/in/Neuroblastoma"},{"id":325790,"name":"Coumarins","url":"https://www.academia.edu/Documents/in/Coumarins"},{"id":361141,"name":"Angiosperms","url":"https://www.academia.edu/Documents/in/Angiosperms"},{"id":469018,"name":"Neoplasms","url":"https://www.academia.edu/Documents/in/Neoplasms"},{"id":470846,"name":"Voltage-Gated Sodium Channels","url":"https://www.academia.edu/Documents/in/Voltage-Gated_Sodium_Channels"},{"id":1953419,"name":"Neuroprotective Agents","url":"https://www.academia.edu/Documents/in/Neuroprotective_Agents"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906356"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906356/Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity"><img alt="Research paper thumbnail of Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906356/Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity">Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity</a></div><div class="wp-workCard_item"><span>Phytotherapy Research</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The purpose of this study was to investigate the antioxidant effects of a hot water extract of Pa...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The purpose of this study was to investigate the antioxidant effects of a hot water extract of Panax notoginseng (PNG) against chronic ethanol-induced hepatotoxicity. Fifty mice were divided into fi ve equal groups with 10 in each group. Group 1 (control) received saline, whereas group 2 received ethanol (70%, 0.1 mL, p.o.) once daily for 4 weeks, which induced hepatotoxicity, manifested biochemically by a significant elevation of serum enzyme activities, such as SGOT and SGPT. Hepatotoxicity was further evidenced by a significant increase in the hepatic lipid peroxidation measured. Groups 3-5 were administered a hot water extract of PNG at doses of 10, 25 and 50 mg/kg 2 weeks after initiating oral administration of ethanol, for a further 2 weeks. PNG ameliorated the rise in serum sGOT and sGPT induced by chronic ethanol administration. The mice were killed after PNG administration. In a separate study, PNG inhibited the lipid peroxidation in the mouse liver homogenate induced by ethanol in a dose-dependent manner. The findings indicate that PNG is an efficient cytoprotective agent against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen-free radicals that cause lipid peroxidation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906356"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906356"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906356; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906356]").text(description); $(".js-view-count[data-work-id=17906356]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906356; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906356']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906356, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906356]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906356,"title":"Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity","translated_title":"","metadata":{"abstract":"The purpose of this study was to investigate the antioxidant effects of a hot water extract of Panax notoginseng (PNG) against chronic ethanol-induced hepatotoxicity. Fifty mice were divided into fi ve equal groups with 10 in each group. Group 1 (control) received saline, whereas group 2 received ethanol (70%, 0.1 mL, p.o.) once daily for 4 weeks, which induced hepatotoxicity, manifested biochemically by a significant elevation of serum enzyme activities, such as SGOT and SGPT. Hepatotoxicity was further evidenced by a significant increase in the hepatic lipid peroxidation measured. Groups 3-5 were administered a hot water extract of PNG at doses of 10, 25 and 50 mg/kg 2 weeks after initiating oral administration of ethanol, for a further 2 weeks. PNG ameliorated the rise in serum sGOT and sGPT induced by chronic ethanol administration. The mice were killed after PNG administration. In a separate study, PNG inhibited the lipid peroxidation in the mouse liver homogenate induced by ethanol in a dose-dependent manner. The findings indicate that PNG is an efficient cytoprotective agent against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen-free radicals that cause lipid peroxidation.","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"Phytotherapy Research"},"translated_abstract":"The purpose of this study was to investigate the antioxidant effects of a hot water extract of Panax notoginseng (PNG) against chronic ethanol-induced hepatotoxicity. Fifty mice were divided into fi ve equal groups with 10 in each group. Group 1 (control) received saline, whereas group 2 received ethanol (70%, 0.1 mL, p.o.) once daily for 4 weeks, which induced hepatotoxicity, manifested biochemically by a significant elevation of serum enzyme activities, such as SGOT and SGPT. Hepatotoxicity was further evidenced by a significant increase in the hepatic lipid peroxidation measured. Groups 3-5 were administered a hot water extract of PNG at doses of 10, 25 and 50 mg/kg 2 weeks after initiating oral administration of ethanol, for a further 2 weeks. PNG ameliorated the rise in serum sGOT and sGPT induced by chronic ethanol administration. The mice were killed after PNG administration. In a separate study, PNG inhibited the lipid peroxidation in the mouse liver homogenate induced by ethanol in a dose-dependent manner. The findings indicate that PNG is an efficient cytoprotective agent against chronic ethanol-induced hepatotoxicity, possibly through inhibition of the production of oxygen-free radicals that cause lipid peroxidation.","internal_url":"https://www.academia.edu/17906356/Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity","translated_internal_url":"","created_at":"2015-11-07T06:50:11.899-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010108,"work_id":17906356,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039515,"email":"c***6@uiuc.edu","display_order":0,"name":"Chi-feng Liu","title":"Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity"},{"id":9010125,"work_id":17906356,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039525,"email":"r***u@www.cmuh.org.tw","display_order":4194304,"name":"Rick Wu","title":"Protection by hot water extract ofPanax notoginseng on chronic ethanol-induced hepatotoxicity"}],"downloadable_attachments":[],"slug":"Protection_by_hot_water_extract_ofPanax_notoginseng_on_chronic_ethanol_induced_hepatotoxicity","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":121705,"name":"Ethanol","url":"https://www.academia.edu/Documents/in/Ethanol"},{"id":260118,"name":"CHEMICAL SCIENCES","url":"https://www.academia.edu/Documents/in/CHEMICAL_SCIENCES"},{"id":269496,"name":"Panax","url":"https://www.academia.edu/Documents/in/Panax"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":1224429,"name":"Drug Induced Liver Injury","url":"https://www.academia.edu/Documents/in/Drug_Induced_Liver_Injury"},{"id":1473454,"name":"Liver function tests","url":"https://www.academia.edu/Documents/in/Liver_function_tests"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906355"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906355/Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity"><img alt="Research paper thumbnail of Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906355/Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity">Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity</a></div><div class="wp-workCard_item"><span>Phytotherapy Research</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect ag...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906355"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906355"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906355; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906355]").text(description); $(".js-view-count[data-work-id=17906355]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906355; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906355']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906355, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906355]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906355,"title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity","translated_title":"","metadata":{"abstract":"The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Phytotherapy Research"},"translated_abstract":"The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.","internal_url":"https://www.academia.edu/17906355/Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity","translated_internal_url":"","created_at":"2015-11-07T06:50:11.795-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010064,"work_id":17906355,"tagging_user_id":37822776,"tagged_user_id":37762182,"co_author_invite_id":null,"email":"l***g@ntnu.edu.tw","display_order":0,"name":"Li-ping Chang","title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity"},{"id":9010084,"work_id":17906355,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":4194304,"name":"Paul Chan","title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity"},{"id":9010110,"work_id":17906355,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039515,"email":"c***6@uiuc.edu","display_order":6291456,"name":"Chi-feng Liu","title":"Antioxidant activity ofGanoderma lucidum in acute ethanol-induced heart toxicity"}],"downloadable_attachments":[],"slug":"Antioxidant_activity_ofGanoderma_lucidum_in_acute_ethanol_induced_heart_toxicity","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":47884,"name":"Biological Sciences","url":"https://www.academia.edu/Documents/in/Biological_Sciences"},{"id":51711,"name":"Antioxidants","url":"https://www.academia.edu/Documents/in/Antioxidants"},{"id":52027,"name":"Phytotherapy","url":"https://www.academia.edu/Documents/in/Phytotherapy"},{"id":84760,"name":"Mice","url":"https://www.academia.edu/Documents/in/Mice"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":121705,"name":"Ethanol","url":"https://www.academia.edu/Documents/in/Ethanol"},{"id":233372,"name":"Lipid peroxidation","url":"https://www.academia.edu/Documents/in/Lipid_peroxidation"},{"id":260118,"name":"CHEMICAL SCIENCES","url":"https://www.academia.edu/Documents/in/CHEMICAL_SCIENCES"},{"id":290433,"name":"Antioxidant Activity","url":"https://www.academia.edu/Documents/in/Antioxidant_Activity"},{"id":354056,"name":"Plant extracts","url":"https://www.academia.edu/Documents/in/Plant_extracts"},{"id":999291,"name":"Reishi","url":"https://www.academia.edu/Documents/in/Reishi"},{"id":1455811,"name":"Superoxides","url":"https://www.academia.edu/Documents/in/Superoxides"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906354"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906354/Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells"><img alt="Research paper thumbnail of Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906354/Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells">Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells</a></div><div class="wp-workCard_item"><span>Pharmacology</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly u...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. The aims of this study were to examine whether isosteviol alters angiotensin-II-induced cell proliferation in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with isosteviol, then stimulated with angiotensin II, after which [(3)H]thymidine incorporation and endothelin-1 secretion were examined. Isosteviol (1-100 micromol/l) inhibits angiotensin-II-induced DNA synthesis and endothelin-1 secretion. Measurements of 2&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;7&amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorofluorescin diacetate, a redox-sensitive fluorescent dye, showed an isosteviol-mediated inhibition of intracellular reactive oxygen species generated by the effects of angiotensin II. The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine. In summary, we speculate that isosteviol inhibits angiotensin-II-induced cell proliferation and endothelin-1 secretion via attenuation of reactive oxygen species generation. Thus, this study provides important insights that may contribute to the effects of isosteviol on the cardiovascular system.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906354"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906354"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906354; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906354]").text(description); $(".js-view-count[data-work-id=17906354]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906354; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906354']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906354, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906354]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906354,"title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells","translated_title":"","metadata":{"abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. The aims of this study were to examine whether isosteviol alters angiotensin-II-induced cell proliferation in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with isosteviol, then stimulated with angiotensin II, after which [(3)H]thymidine incorporation and endothelin-1 secretion were examined. Isosteviol (1-100 micromol/l) inhibits angiotensin-II-induced DNA synthesis and endothelin-1 secretion. Measurements of 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorofluorescin diacetate, a redox-sensitive fluorescent dye, showed an isosteviol-mediated inhibition of intracellular reactive oxygen species generated by the effects of angiotensin II. The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine. In summary, we speculate that isosteviol inhibits angiotensin-II-induced cell proliferation and endothelin-1 secretion via attenuation of reactive oxygen species generation. Thus, this study provides important insights that may contribute to the effects of isosteviol on the cardiovascular system.","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"Pharmacology"},"translated_abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. The aims of this study were to examine whether isosteviol alters angiotensin-II-induced cell proliferation in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with isosteviol, then stimulated with angiotensin II, after which [(3)H]thymidine incorporation and endothelin-1 secretion were examined. Isosteviol (1-100 micromol/l) inhibits angiotensin-II-induced DNA synthesis and endothelin-1 secretion. Measurements of 2\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;7\u0026amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;#39;-dichlorofluorescin diacetate, a redox-sensitive fluorescent dye, showed an isosteviol-mediated inhibition of intracellular reactive oxygen species generated by the effects of angiotensin II. The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine. In summary, we speculate that isosteviol inhibits angiotensin-II-induced cell proliferation and endothelin-1 secretion via attenuation of reactive oxygen species generation. Thus, this study provides important insights that may contribute to the effects of isosteviol on the cardiovascular system.","internal_url":"https://www.academia.edu/17906354/Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.701-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010030,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1564394,"email":"j***n@mail.cmu.edu.tw","display_order":0,"name":"Jaung-geng Lin","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010031,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1054925,"email":"t***g@mail.cmu.edu.tw","display_order":4194304,"name":"Tzu-hurng Cheng","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010094,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":612359,"email":"w***u@tmu.edu.tw","display_order":6291456,"name":"Wen-ta Chiu","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010095,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039507,"email":"s***h@ndmctsgh.edu.tw","display_order":7340032,"name":"Shih-hurng Loh","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010101,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039511,"email":"h***y@tmu.edu.tw","display_order":7864320,"name":"Cheng-hsien Chen","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"},{"id":9010122,"work_id":17906354,"tagging_user_id":37822776,"tagged_user_id":40674726,"co_author_invite_id":1211305,"email":"l***2@ndmctsgh.edu.tw","display_order":8126464,"name":"Li-ling Lin","title":"Antiproliferative Effect of Isosteviol on Angiotensin-II-Treated Rat Aortic Smooth Muscle Cells"}],"downloadable_attachments":[],"slug":"Antiproliferative_Effect_of_Isosteviol_on_Angiotensin_II_Treated_Rat_Aortic_Smooth_Muscle_Cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":140,"name":"Pharmacology","url":"https://www.academia.edu/Documents/in/Pharmacology"},{"id":82978,"name":"Reactive Oxygen 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</script> <div class="js-work-strip profile--work_container" data-work-id="17767103"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17767103/Midazolam_induces_apoptosis_in_MA_10_mouse_Leydig_tumor_cells_through_caspase_activation_and_the_involvement_of_MAPK_signaling_pathway"><img alt="Research paper thumbnail of Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway" class="work-thumbnail" src="https://attachments.academia-assets.com/39698189/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17767103/Midazolam_induces_apoptosis_in_MA_10_mouse_Leydig_tumor_cells_through_caspase_activation_and_the_involvement_of_MAPK_signaling_pathway">Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://ncku.academia.edu/YWang">Yang-Kao Wang</a>, <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a>, and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a></span></div><div class="wp-workCard_item"><span>OncoTargets and Therapy</span><span>, 2014</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c22141809d786dde86742aad5595f034" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39698189,"asset_id":17767103,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39698189/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17767103"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" 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new Works.PaperRankView({ workId: 17767103, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "c22141809d786dde86742aad5595f034" } } $('.js-work-strip[data-work-id=17767103]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17767103,"title":"Midazolam induces apoptosis in MA-10 mouse Leydig tumor cells through caspase activation and the involvement of 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dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906353"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906353/Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat"><img alt="Research paper thumbnail of Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906353/Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat">Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat</a></div><div class="wp-workCard_item"><span>Life Sciences</span><span>, 2004</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly u...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. In the present study, the role of potassium channels in the vasodilator effect of isosteviol was investigated using potassium channel blockers on isosteviol-induced relaxation of isolated aortic rings prepared from Wistar rats. Isosteviol dose-dependently relaxed the vasopressin (10(-8) M)-induced vasoconstriction in isolated aortic rings with or without endothelium. However, in the presence of potassium chloride (3x10(-2) M), the vasodilator effect of isosteviol on arterial strips disappeared. Only the inhibitors specific for the ATP-sensitive potassium (K(ATP)) channel or small conductance calcium-activated potassium (SK(Ca)) channel inhibited the vasodilator effect of isosteviol in isolated aortic rings contracted with 10(-8) M vasopressin. Also; since the isosteviol-induced relaxation was unchanged by methylene blue, a role of nitric oxide and/or endothelium in the vasodilatation produced by isosteviol could be ruled out. The obtained results indicated that vasodilatation induced by isosteviol is related to the opening of SK(Ca) and K(ATP) channels.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906353"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906353"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906353; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906353]").text(description); $(".js-view-count[data-work-id=17906353]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906353; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906353']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906353, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906353]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906353,"title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat","translated_title":"","metadata":{"abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. In the present study, the role of potassium channels in the vasodilator effect of isosteviol was investigated using potassium channel blockers on isosteviol-induced relaxation of isolated aortic rings prepared from Wistar rats. Isosteviol dose-dependently relaxed the vasopressin (10(-8) M)-induced vasoconstriction in isolated aortic rings with or without endothelium. However, in the presence of potassium chloride (3x10(-2) M), the vasodilator effect of isosteviol on arterial strips disappeared. Only the inhibitors specific for the ATP-sensitive potassium (K(ATP)) channel or small conductance calcium-activated potassium (SK(Ca)) channel inhibited the vasodilator effect of isosteviol in isolated aortic rings contracted with 10(-8) M vasopressin. Also; since the isosteviol-induced relaxation was unchanged by methylene blue, a role of nitric oxide and/or endothelium in the vasodilatation produced by isosteviol could be ruled out. The obtained results indicated that vasodilatation induced by isosteviol is related to the opening of SK(Ca) and K(ATP) channels.","publication_date":{"day":null,"month":null,"year":2004,"errors":{}},"publication_name":"Life Sciences"},"translated_abstract":"Isosteviol is a derivative of stevioside, a constituent of Stevia rebaudiana, which is commonly used as a noncaloric sugar substitute in Japan and Brazil. In the present study, the role of potassium channels in the vasodilator effect of isosteviol was investigated using potassium channel blockers on isosteviol-induced relaxation of isolated aortic rings prepared from Wistar rats. Isosteviol dose-dependently relaxed the vasopressin (10(-8) M)-induced vasoconstriction in isolated aortic rings with or without endothelium. However, in the presence of potassium chloride (3x10(-2) M), the vasodilator effect of isosteviol on arterial strips disappeared. Only the inhibitors specific for the ATP-sensitive potassium (K(ATP)) channel or small conductance calcium-activated potassium (SK(Ca)) channel inhibited the vasodilator effect of isosteviol in isolated aortic rings contracted with 10(-8) M vasopressin. Also; since the isosteviol-induced relaxation was unchanged by methylene blue, a role of nitric oxide and/or endothelium in the vasodilatation produced by isosteviol could be ruled out. The obtained results indicated that vasodilatation induced by isosteviol is related to the opening of SK(Ca) and K(ATP) channels.","internal_url":"https://www.academia.edu/17906353/Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat","translated_internal_url":"","created_at":"2015-11-07T06:50:11.527-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010037,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":118320,"email":"e***m@hindawi.com","display_order":0,"name":"I-min Liu","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"},{"id":9010042,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":4194304,"name":"Juei-tang Cheng","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"},{"id":9010066,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":37939559,"co_author_invite_id":836505,"email":"h***0@tmu.edu.tw","display_order":6291456,"name":"H.-h. Hsu","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"},{"id":9010085,"work_id":17906353,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":7340032,"name":"Paul Chan","title":"Isosteviol acts on potassium channels to relax isolated aortic strips of Wistar rat"}],"downloadable_attachments":[],"slug":"Isosteviol_acts_on_potassium_channels_to_relax_isolated_aortic_strips_of_Wistar_rat","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":8014,"name":"Life Sciences","url":"https://www.academia.edu/Documents/in/Life_Sciences"},{"id":93922,"name":"Nitric oxide","url":"https://www.academia.edu/Documents/in/Nitric_oxide"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":138877,"name":"Vascular endothelium","url":"https://www.academia.edu/Documents/in/Vascular_endothelium"},{"id":160656,"name":"Potassium","url":"https://www.academia.edu/Documents/in/Potassium"},{"id":196381,"name":"Methylene Blue","url":"https://www.academia.edu/Documents/in/Methylene_Blue"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":416452,"name":"Diterpenes","url":"https://www.academia.edu/Documents/in/Diterpenes"},{"id":557691,"name":"Potassium Channels","url":"https://www.academia.edu/Documents/in/Potassium_Channels"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":1035092,"name":"Aorta","url":"https://www.academia.edu/Documents/in/Aorta"},{"id":1035420,"name":"Vasodilation","url":"https://www.academia.edu/Documents/in/Vasodilation"},{"id":1295914,"name":"Potassium Chloride","url":"https://www.academia.edu/Documents/in/Potassium_Chloride"},{"id":1621878,"name":"Guanylate Cyclase","url":"https://www.academia.edu/Documents/in/Guanylate_Cyclase"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1724844,"name":"Molecular Structure","url":"https://www.academia.edu/Documents/in/Molecular_Structure"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906352"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906352/l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_"><img alt="Research paper thumbnail of l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906352/l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_">l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆</a></div><div class="wp-workCard_item"><span>The Journal of Nutritional Biochemistry</span><span>, 2010</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provid...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provided by the blood stream; however, additional studies are needed to better understand the mechanism of L-carnitine supplementation to the heart. The aim of this study was to evaluate the effects of L-carnitine on angiotensin II (Ang II)-induced cardiac fibroblast proliferation and to explore its intracellular mechanism(s). Cultured rat cardiac fibroblasts were pretreated with L-carnitine (1-30 mM) then stimulated with Ang II (100 nM). Ang II increased fibroblast proliferation and endothelin-1 expression, which were partially inhibited by L-carnitine. L-carnitine also attenuated Ang II-induced NADPH oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, activator protein-1-mediated reporter activity and sphingosine-1-phosphate generation. In addition, L-carnitine increased prostacyclin (PGI(2)) generation in cardiac fibroblasts. siRNA transfection of PGI(2) synthase significantly reduced L-carnitine-induced PGI(2) and its anti-proliferation effects on cardiac fibroblasts. Furthermore, blockading potential PGI(2) receptors, including immunoprecipitation (IP) receptors and peroxisome proliferator-activated receptors alpha (PPAR alpha) and delta, revealed that siRNA-mediated blockage of PPAR alpha considerably reduced the anti-proliferation effect of L-carnitine. In summary, these results suggest that L-carnitine attenuates Ang II-induced effects (including NADPH oxidase activation, sphingosine-1-phosphate generation and cell proliferation) in part through PGI(2) and PPAR alpha-signaling pathways.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906352"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906352"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906352; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906352]").text(description); $(".js-view-count[data-work-id=17906352]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906352; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906352']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906352, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906352]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906352,"title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆","translated_title":"","metadata":{"abstract":"The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provided by the blood stream; however, additional studies are needed to better understand the mechanism of L-carnitine supplementation to the heart. The aim of this study was to evaluate the effects of L-carnitine on angiotensin II (Ang II)-induced cardiac fibroblast proliferation and to explore its intracellular mechanism(s). Cultured rat cardiac fibroblasts were pretreated with L-carnitine (1-30 mM) then stimulated with Ang II (100 nM). Ang II increased fibroblast proliferation and endothelin-1 expression, which were partially inhibited by L-carnitine. L-carnitine also attenuated Ang II-induced NADPH oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, activator protein-1-mediated reporter activity and sphingosine-1-phosphate generation. In addition, L-carnitine increased prostacyclin (PGI(2)) generation in cardiac fibroblasts. siRNA transfection of PGI(2) synthase significantly reduced L-carnitine-induced PGI(2) and its anti-proliferation effects on cardiac fibroblasts. Furthermore, blockading potential PGI(2) receptors, including immunoprecipitation (IP) receptors and peroxisome proliferator-activated receptors alpha (PPAR alpha) and delta, revealed that siRNA-mediated blockage of PPAR alpha considerably reduced the anti-proliferation effect of L-carnitine. In summary, these results suggest that L-carnitine attenuates Ang II-induced effects (including NADPH oxidase activation, sphingosine-1-phosphate generation and cell proliferation) in part through PGI(2) and PPAR alpha-signaling pathways.","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"The Journal of Nutritional Biochemistry"},"translated_abstract":"The heart is unable to synthesize L-carnitine and is strictly dependent on the L-carnitine provided by the blood stream; however, additional studies are needed to better understand the mechanism of L-carnitine supplementation to the heart. The aim of this study was to evaluate the effects of L-carnitine on angiotensin II (Ang II)-induced cardiac fibroblast proliferation and to explore its intracellular mechanism(s). Cultured rat cardiac fibroblasts were pretreated with L-carnitine (1-30 mM) then stimulated with Ang II (100 nM). Ang II increased fibroblast proliferation and endothelin-1 expression, which were partially inhibited by L-carnitine. L-carnitine also attenuated Ang II-induced NADPH oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, activator protein-1-mediated reporter activity and sphingosine-1-phosphate generation. In addition, L-carnitine increased prostacyclin (PGI(2)) generation in cardiac fibroblasts. siRNA transfection of PGI(2) synthase significantly reduced L-carnitine-induced PGI(2) and its anti-proliferation effects on cardiac fibroblasts. Furthermore, blockading potential PGI(2) receptors, including immunoprecipitation (IP) receptors and peroxisome proliferator-activated receptors alpha (PPAR alpha) and delta, revealed that siRNA-mediated blockage of PPAR alpha considerably reduced the anti-proliferation effect of L-carnitine. In summary, these results suggest that L-carnitine attenuates Ang II-induced effects (including NADPH oxidase activation, sphingosine-1-phosphate generation and cell proliferation) in part through PGI(2) and PPAR alpha-signaling pathways.","internal_url":"https://www.academia.edu/17906352/l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_","translated_internal_url":"","created_at":"2015-11-07T06:50:11.436-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010035,"work_id":17906352,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1054925,"email":"t***g@mail.cmu.edu.tw","display_order":0,"name":"Tzu-hurng Cheng","title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆"},{"id":9010103,"work_id":17906352,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039511,"email":"h***y@tmu.edu.tw","display_order":4194304,"name":"Cheng-hsien Chen","title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆"},{"id":9010123,"work_id":17906352,"tagging_user_id":37822776,"tagged_user_id":40674726,"co_author_invite_id":1211305,"email":"l***2@ndmctsgh.edu.tw","display_order":6291456,"name":"Li-ling Lin","title":"l-Carnitine attenuates angiotensin II-induced proliferation of cardiac fibroblasts: role of NADPH oxidase inhibition and decreased sphingosine-1-phosphate generation☆"}],"downloadable_attachments":[],"slug":"l_Carnitine_attenuates_angiotensin_II_induced_proliferation_of_cardiac_fibroblasts_role_of_NADPH_oxidase_inhibition_and_decreased_sphingosine_1_phosphate_generation_","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":591,"name":"Nutrition and Dietetics","url":"https://www.academia.edu/Documents/in/Nutrition_and_Dietetics"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":82978,"name":"Reactive Oxygen Species","url":"https://www.academia.edu/Documents/in/Reactive_Oxygen_Species"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":131495,"name":"Heart","url":"https://www.academia.edu/Documents/in/Heart"},{"id":172083,"name":"Phosphorylation","url":"https://www.academia.edu/Documents/in/Phosphorylation"},{"id":234980,"name":"NADPH oxidase","url":"https://www.academia.edu/Documents/in/NADPH_oxidase"},{"id":295453,"name":"L-carnitine","url":"https://www.academia.edu/Documents/in/L-carnitine"},{"id":298041,"name":"Nutritional Biochemistry","url":"https://www.academia.edu/Documents/in/Nutritional_Biochemistry"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":392828,"name":"Myocardium","url":"https://www.academia.edu/Documents/in/Myocardium"},{"id":539690,"name":"Endothelin-1","url":"https://www.academia.edu/Documents/in/Endothelin-1"},{"id":573653,"name":"Food Sciences","url":"https://www.academia.edu/Documents/in/Food_Sciences"},{"id":782251,"name":"Cell Proliferation","url":"https://www.academia.edu/Documents/in/Cell_Proliferation"},{"id":954841,"name":"Angiotensin II","url":"https://www.academia.edu/Documents/in/Angiotensin_II"},{"id":954995,"name":"Human Fibroblasts","url":"https://www.academia.edu/Documents/in/Human_Fibroblasts"},{"id":1361338,"name":"Sphingosine 1-phosphate","url":"https://www.academia.edu/Documents/in/Sphingosine_1-phosphate"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":1763968,"name":"Gene Expression Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"},{"id":2003019,"name":"Sphingosine","url":"https://www.academia.edu/Documents/in/Sphingosine"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906351"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906351/Use_of_condoms_as_blade_covers_during_laryngoscopy_a_method_to_reduce_possible_cross_infection_among_patients"><img alt="Research paper thumbnail of Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients" class="work-thumbnail" src="https://attachments.academia-assets.com/39773303/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906351/Use_of_condoms_as_blade_covers_during_laryngoscopy_a_method_to_reduce_possible_cross_infection_among_patients">Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a></span></div><div class="wp-workCard_item"><span>Journal of Infection</span><span>, 2006</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="513fcbc9adf12945c5223b8056d564e7" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773303,"asset_id":17906351,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773303/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906351"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906351"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906351; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906351]").text(description); $(".js-view-count[data-work-id=17906351]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906351; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906351']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906351, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "513fcbc9adf12945c5223b8056d564e7" } } $('.js-work-strip[data-work-id=17906351]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906351,"title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients","translated_title":"","metadata":{"grobid_abstract":"Objectives: Laryngoscope blades are in close contact with mucous membranes and can possibly contaminated with virulent or readily transmissible organisms. As laryngoscopy is often required during endotracheal intubation, proper cleaning and sterilization of the laryngoscope blade is crucial to prevent crosscontamination among patients. Methods: We tested the effectiveness of latex condom using as a laryngoscope blade cover during endotracheal intubation. Both control (no condom) and study group blades were rinsed with sterile saline after intubation. The rinse was sent for bacteria culture, and appearance of bacterial colonization was counted as positive. A water leak test (WLT) was performed on used condoms to verify their integrity. Results: There were total 162 laryngoscopes studied with 83 (51.2%) scopes in the study group and 79 (48.8%) in the control group. Rate of positive bacterial culture were 13.3% and 88.6% in the study and control group, respectively. Although WLT (C) rate of 41% was found in the study group, a high negative culture rate (71.6%) was also noted among the WLT (C) group. Conclusions: Condom when using as a blade cover during laryngoscopy is a simple, inexpansive and effective way in reducing cross contamination among patients.","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"Journal of Infection","grobid_abstract_attachment_id":39773303},"translated_abstract":null,"internal_url":"https://www.academia.edu/17906351/Use_of_condoms_as_blade_covers_during_laryngoscopy_a_method_to_reduce_possible_cross_infection_among_patients","translated_internal_url":"","created_at":"2015-11-07T06:50:11.342-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010028,"work_id":17906351,"tagging_user_id":37822776,"tagged_user_id":37925459,"co_author_invite_id":1975987,"email":"e***w@gmail.com","affiliation":"China Medical University,Taiwan","display_order":0,"name":"Edmund So","title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients"},{"id":9010076,"work_id":17906351,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1958426,"email":"c***h@hotmail.com","display_order":4194304,"name":"Yin-ching Chuang","title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among patients"},{"id":9010121,"work_id":17906351,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039523,"email":"y***g@mail.ukn.edu.tw","display_order":6291456,"name":"Yi-chueh Yang","title":"Use of condoms as blade covers during laryngoscopy, a method to reduce possible cross infection among 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Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[{"id":39773303,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/39773303/thumbnails/1.jpg","file_name":"j.jinf.2005.03.004.pdf20151107-4773-122tvp8","download_url":"https://www.academia.edu/attachments/39773303/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Use_of_condoms_as_blade_covers_during_la.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/39773303/j.jinf.2005.03.004-libre.pdf20151107-4773-122tvp8?1446907895=\u0026response-content-disposition=attachment%3B+filename%3DUse_of_condoms_as_blade_covers_during_la.pdf\u0026Expires=1732272203\u0026Signature=DcRpLehFzxDSgmMCCP1eRD6YQdthZTP27bu24LqlNp8Y4woUyBHgdzgK2oMmGyz09wA3A4hKUH5xBiWWqhyDlAi8bpw7UwC912ZD5he-eu-kY8mzhz-DW6WvKSfrQml1WvT49hJ8k0Q5Vej5qSpR3R6kzzMg43dxXBpFcE-QtWgM0Y6OSFR0x0NiEQYRlyMJM~tJvInUrNmJIY1x9AegLURGtKx50w4xtIHjcE5KbftKknRZhXi0tCKbpjqv-VCts72gN7d8DRuhsTCDs7GLhft2hAE27szwZ-EJjL8ueD4noa-4JA1NOsNcU4N9dvmmhpWUxZVgSrrlxzYXu-9a4Q__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":55155,"name":"Emergency Medical Services","url":"https://www.academia.edu/Documents/in/Emergency_Medical_Services"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":109739,"name":"Infection","url":"https://www.academia.edu/Documents/in/Infection"},{"id":177876,"name":"Sterilization","url":"https://www.academia.edu/Documents/in/Sterilization"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":474853,"name":"Operating Rooms","url":"https://www.academia.edu/Documents/in/Operating_Rooms"},{"id":988244,"name":"Condoms","url":"https://www.academia.edu/Documents/in/Condoms"},{"id":1206482,"name":"Cross-infection","url":"https://www.academia.edu/Documents/in/Cross-infection"},{"id":1747358,"name":"Laryngoscopy","url":"https://www.academia.edu/Documents/in/Laryngoscopy"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906350"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906350/Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats"><img alt="Research paper thumbnail of Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906350/Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats">Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats</a></div><div class="wp-workCard_item"><span>Journal of Hypertension</span><span>, 2003</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) receptor subtype, to investigate the effect of AT(1) receptor on the plasma glucose metabolism in streptozotocin-induced diabetic rats (STZ-diabetic rats). The plasma glucose concentration was assessed by glucose oxidase method and plasma insulin was measured using enzyme-linked immunosorbent assay. Systolic blood pressure (SBP) was determined by the tail-cuff method. The intravenous glucose challenge test (IVGCT) was carried out to evaluate the effect of valsartan on the glucose utilization in vivo. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis. Moreover, the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Plasma glucose-lowering action of valsartan also observed in normal rats although in a way not so effective as that in STZ-diabetic rats. Valsartan at the dose of 0.2 mg/kg that produced the maximal plasma glucose-lowering activity in STZ-diabetic rats is also effective to lower the SBP. However, oral treatment with nifedipine or nicorandil in STZ-diabetic rats at the dose sufficient to decrease SBP showed no change of plasma glucose. Otherwise, infusion of saralasin (10 microg/kg per min) into STZ-diabetic rats produced a plasma glucose-lowering activity similar to that by valsartan at 0.2 mg/kg. Moreover, valsartan (0.2 mg/kg) significantly attenuated the raise of plasma glucose induced by IVGCT in normal rats. Repeated intravenous administration of valsartan (0.2 mg/kg) in STZ-diabetic rats resulted in the lowering of plasma glucose after 3 days. The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days. Moreover, similar repeated treatment with valsartan reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. These results suggest that the plasma glucose-lowering activity of AT(1) receptor antagonism was associated with an increase in the glucose utilization in peripheral tissue and/or a reduction in hepatic gluconeogenesis in the absence of insulin.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906350"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906350"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906350; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906350]").text(description); $(".js-view-count[data-work-id=17906350]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906350; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906350']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906350, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906350]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906350,"title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats","translated_title":"","metadata":{"abstract":"In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) receptor subtype, to investigate the effect of AT(1) receptor on the plasma glucose metabolism in streptozotocin-induced diabetic rats (STZ-diabetic rats). The plasma glucose concentration was assessed by glucose oxidase method and plasma insulin was measured using enzyme-linked immunosorbent assay. Systolic blood pressure (SBP) was determined by the tail-cuff method. The intravenous glucose challenge test (IVGCT) was carried out to evaluate the effect of valsartan on the glucose utilization in vivo. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis. Moreover, the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Plasma glucose-lowering action of valsartan also observed in normal rats although in a way not so effective as that in STZ-diabetic rats. Valsartan at the dose of 0.2 mg/kg that produced the maximal plasma glucose-lowering activity in STZ-diabetic rats is also effective to lower the SBP. However, oral treatment with nifedipine or nicorandil in STZ-diabetic rats at the dose sufficient to decrease SBP showed no change of plasma glucose. Otherwise, infusion of saralasin (10 microg/kg per min) into STZ-diabetic rats produced a plasma glucose-lowering activity similar to that by valsartan at 0.2 mg/kg. Moreover, valsartan (0.2 mg/kg) significantly attenuated the raise of plasma glucose induced by IVGCT in normal rats. Repeated intravenous administration of valsartan (0.2 mg/kg) in STZ-diabetic rats resulted in the lowering of plasma glucose after 3 days. The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days. Moreover, similar repeated treatment with valsartan reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. These results suggest that the plasma glucose-lowering activity of AT(1) receptor antagonism was associated with an increase in the glucose utilization in peripheral tissue and/or a reduction in hepatic gluconeogenesis in the absence of insulin.","publication_date":{"day":null,"month":null,"year":2003,"errors":{}},"publication_name":"Journal of Hypertension"},"translated_abstract":"In the present study, we use valsartan, a highly selective antagonist for angiotensin(1) (AT(1)) receptor subtype, to investigate the effect of AT(1) receptor on the plasma glucose metabolism in streptozotocin-induced diabetic rats (STZ-diabetic rats). The plasma glucose concentration was assessed by glucose oxidase method and plasma insulin was measured using enzyme-linked immunosorbent assay. Systolic blood pressure (SBP) was determined by the tail-cuff method. The intravenous glucose challenge test (IVGCT) was carried out to evaluate the effect of valsartan on the glucose utilization in vivo. The mRNA levels of the subtype 4 form of glucose transporter (GLUT4) in soleus muscle and phosphoenolpyruvate carboxykinase (PEPCK) in the liver were detected by Northern blotting analysis. Moreover, the protein levels of GLUT4 in isolated soleus muscle and hepatic PEPCK were investigated using Western blotting analysis. A single intravenous injection of valsartan decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Plasma glucose-lowering action of valsartan also observed in normal rats although in a way not so effective as that in STZ-diabetic rats. Valsartan at the dose of 0.2 mg/kg that produced the maximal plasma glucose-lowering activity in STZ-diabetic rats is also effective to lower the SBP. However, oral treatment with nifedipine or nicorandil in STZ-diabetic rats at the dose sufficient to decrease SBP showed no change of plasma glucose. Otherwise, infusion of saralasin (10 microg/kg per min) into STZ-diabetic rats produced a plasma glucose-lowering activity similar to that by valsartan at 0.2 mg/kg. Moreover, valsartan (0.2 mg/kg) significantly attenuated the raise of plasma glucose induced by IVGCT in normal rats. Repeated intravenous administration of valsartan (0.2 mg/kg) in STZ-diabetic rats resulted in the lowering of plasma glucose after 3 days. The mRNA and protein levels of GLUT4 in the soleus muscle were increased after repeated intravenous administration of valsartan in STZ-diabetic rats for 3 days. Moreover, similar repeated treatment with valsartan reversed the elevated mRNA and protein levels of PEPCK in the liver of STZ-diabetic rats. These results suggest that the plasma glucose-lowering activity of AT(1) receptor antagonism was associated with an increase in the glucose utilization in peripheral tissue and/or a reduction in hepatic gluconeogenesis in the absence of insulin.","internal_url":"https://www.academia.edu/17906350/Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats","translated_internal_url":"","created_at":"2015-11-07T06:50:11.266-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010036,"work_id":17906350,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":118320,"email":"e***m@hindawi.com","display_order":0,"name":"I-min Liu","title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats"},{"id":9010040,"work_id":17906350,"tagging_user_id":37822776,"tagged_user_id":38847042,"co_author_invite_id":2039499,"email":"j***g@mail.ncku.edu.tw","display_order":4194304,"name":"Juei-tang Cheng","title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats"},{"id":9010081,"work_id":17906350,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1308574,"email":"c***l@wanfang.gov.tw","display_order":6291456,"name":"Paul Chan","title":"Antihyperglycemic action of angiotensin II receptor antagonist, valsartan, in streptozotocin-induced diabetic rats"}],"downloadable_attachments":[],"slug":"Antihyperglycemic_action_of_angiotensin_II_receptor_antagonist_valsartan_in_streptozotocin_induced_diabetic_rats","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[],"research_interests":[{"id":4228,"name":"Skeletal muscle biology","url":"https://www.academia.edu/Documents/in/Skeletal_muscle_biology"},{"id":27784,"name":"Gene expression","url":"https://www.academia.edu/Documents/in/Gene_expression"},{"id":71290,"name":"Hyperglycemia","url":"https://www.academia.edu/Documents/in/Hyperglycemia"},{"id":71300,"name":"Blood Glucose","url":"https://www.academia.edu/Documents/in/Blood_Glucose"},{"id":71399,"name":"Hypertension","url":"https://www.academia.edu/Documents/in/Hypertension"},{"id":71437,"name":"Liver","url":"https://www.academia.edu/Documents/in/Liver"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":111545,"name":"Male","url":"https://www.academia.edu/Documents/in/Male"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":564879,"name":"Wistar Rats","url":"https://www.academia.edu/Documents/in/Wistar_Rats"},{"id":790002,"name":"Streptozotocin","url":"https://www.academia.edu/Documents/in/Streptozotocin"},{"id":901298,"name":"Glucose Tolerance Test","url":"https://www.academia.edu/Documents/in/Glucose_Tolerance_Test"},{"id":915951,"name":"Type 2 Diabetes Mellitus","url":"https://www.academia.edu/Documents/in/Type_2_Diabetes_Mellitus"},{"id":1029499,"name":"Nifedipine","url":"https://www.academia.edu/Documents/in/Nifedipine"},{"id":1031967,"name":"Diabetic Rat","url":"https://www.academia.edu/Documents/in/Diabetic_Rat"},{"id":1954221,"name":"Calcium Channel Blockers","url":"https://www.academia.edu/Documents/in/Calcium_Channel_Blockers"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906349"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906349/Hypoxia_induced_matrix_metalloproteinase_13_expression_in_astrocytes_enhances_permeability_of_brain_endothelial_cells"><img alt="Research paper thumbnail of Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells" class="work-thumbnail" src="https://attachments.academia-assets.com/39773304/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906349/Hypoxia_induced_matrix_metalloproteinase_13_expression_in_astrocytes_enhances_permeability_of_brain_endothelial_cells">Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells</a></div><div class="wp-workCard_item"><span>Journal of Cellular Physiology</span><span>, 2009</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="7622911da6d8dd4616b7cba16edb9dd6" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773304,"asset_id":17906349,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773304/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906349"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906349"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906349; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906349]").text(description); $(".js-view-count[data-work-id=17906349]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906349; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906349']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906349, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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Here we found that hypoxia increased MMP-13 protein and mRNA levels in primary rat astrocyte cultures. Hypoxia stimulation also increased the secretion of MMP-13 from astrocytes, as shown by zymographic analysis. In addition, exposure to hypoxia up-regulated the expression of c-Fos and c-Jun time-dependently. Hypoxia-induced MMP-13 overexpression was antagonized by transfection with antisense oligodeoxynucleotides (AS-ODN) of c-Fos or c-Jun. Furthermore, hypoxic-conditioned medium (Hx-CM) collected from astrocytes exposed to hypoxia increased paracellular permeability of adult rat brain endothelial cells (ARBECs). Administration of MMP-13 neutralizing antibody antagonized Hx-CM-induced paracellular permeability of ARBECs. Furthermore, pre-transfection of astrocytes with AS-ODN of c-Fos, c-Jun or MMP-13-shRNA significantly decreased hyperpermeability of ARBECs induced by Hx-CM. The arrangement of tight junction protein (TJP) zonular occludens-1 (ZO-1) of ARBECs disorganized in response to Hx-CM. Administration of Hx-CM to ARBECs also resulted in the production of proteolytic fragments of ZO-1, which was antagonized by transfection of MMP-13-shRNA in primary astrocytes. Administration of MMP-13 recombinant protein to ARBECs led to the disorganization and fragmentation of ZO-1 protein and also increased paracellular permeability. These results suggest that hypoxia-induced MMP-13 expression in astrocytes is regulated by c-Fos and c-Jun. MMP-13 is an important factor leading to the disorganization of ZO-1 and hyperpermeablility of blood-brain barrier in response to hypoxia.","publication_date":{"day":null,"month":null,"year":2009,"errors":{}},"publication_name":"Journal of Cellular Physiology","grobid_abstract_attachment_id":39773304},"translated_abstract":null,"internal_url":"https://www.academia.edu/17906349/Hypoxia_induced_matrix_metalloproteinase_13_expression_in_astrocytes_enhances_permeability_of_brain_endothelial_cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.184-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010048,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039500,"email":"d***u@mail.cmu.edu.tw","display_order":0,"name":"Dah-yuu Lu","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells"},{"id":9010057,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":4194304,"name":"Yuk-man Leung","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells"},{"id":9010072,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1946164,"email":"c***l@mail.cmu.edu.tw","display_order":6291456,"name":"Chih-ho Lai","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial cells"},{"id":9010074,"work_id":17906349,"tagging_user_id":37822776,"tagged_user_id":263183925,"co_author_invite_id":2039502,"email":"w***i@ntu.edu.tw","display_order":7340032,"name":"Wen-mei Fu","title":"Hypoxia-induced matrix metalloproteinase-13 expression in astrocytes enhances permeability of brain endothelial 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906348"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906348/Bradykinin_induced_cell_migration_and_COX_2_production_mediated_by_the_bradykinin_B1_receptor_in_glioma_cells"><img alt="Research paper thumbnail of Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells" class="work-thumbnail" src="https://attachments.academia-assets.com/39773302/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906348/Bradykinin_induced_cell_migration_and_COX_2_production_mediated_by_the_bradykinin_B1_receptor_in_glioma_cells">Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells</a></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2010</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="1b4988d1e3b70267e8782e9aad6a1870" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":39773302,"asset_id":17906348,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/39773302/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906348"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906348"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906348; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906348]").text(description); $(".js-view-count[data-work-id=17906348]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x 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window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "1b4988d1e3b70267e8782e9aad6a1870" } } $('.js-work-strip[data-work-id=17906348]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906348,"title":"Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells","translated_title":"","metadata":{"grobid_abstract":"Bradykinin is produced and acts at the site of injury and inflammation. Recent reports have also shown that bradykinin selectively modulates blood-tumor barrier permeability. However, the molecular mechanisms and pathologic roles underlying bradykinin-induced glioma migration remain unclear. Glioma is the most common primary adult brain tumor, with a poor prognosis because of the ease with which tumor cells spread to other regions of the brain. In this study, we found that bradykinin increases the cell migration and expression of cyclooxygenase-2 (COX-2) in glioma cells. Bradykinin-mediated migration was attenuated by the selective COX-2 inhibitor NS-398. Moreover, increased motility of glioma cells and expression of COX-2 were mimicked by a bradykinin B1 receptor (B1R) agonist and markedly inhibited by a B1R antagonist. Bradykinin-mediated migration was attenuated by phosphoinositide 3-kinase (PI-3 kinase)/AKT inhibitors LY 294002 and wortmannin. Bradykinin stimulation also increased the phosphorylation of the p85 subunit of PI-3 kinase and serine 473 of AKT. Treatment of bradykinin with AP-1 inhibitors Tanshinone IIA and curcumin also reduced COX-2 expression and glioma cell migration. Moreover, treatment of bradykinin also induced phosphorylation of c-Jun in glioma cells. AP-1 promoter analysis in the luciferase reporter construct showed that bradykinin increased AP-1 transcription activity and was inhibited by LY 294002 and wortmannin. One mechanism underlying bradykinin-directed migration is transcriptional up-regulation of COX-2 and activation of the B1R receptor, PI-3 kinase, AKT, c-Jun, and AP-1 pathways.","publication_date":{"day":null,"month":null,"year":2010,"errors":{}},"publication_name":"Journal of Cellular Biochemistry","grobid_abstract_attachment_id":39773302},"translated_abstract":null,"internal_url":"https://www.academia.edu/17906348/Bradykinin_induced_cell_migration_and_COX_2_production_mediated_by_the_bradykinin_B1_receptor_in_glioma_cells","translated_internal_url":"","created_at":"2015-11-07T06:50:11.100-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010046,"work_id":17906348,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039500,"email":"d***u@mail.cmu.edu.tw","display_order":0,"name":"Dah-yuu Lu","title":"Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells"},{"id":9010054,"work_id":17906348,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":1458717,"email":"y***g@mail.cmu.edu.tw","display_order":4194304,"name":"Yuk-man Leung","title":"Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells"},{"id":9010111,"work_id":17906348,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2039516,"email":"s***g@phys.sinica.edu.tw","display_order":6291456,"name":"Ssu-ming Huang","title":"Bradykinin-induced cell migration and COX-2 production mediated by the bradykinin B1 receptor in glioma cells"}],"downloadable_attachments":[{"id":39773302,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/39773302/thumbnails/1.jpg","file_name":"jcb.22520.pdf20151107-4768-1o00gty","download_url":"https://www.academia.edu/attachments/39773302/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Bradykinin_induced_cell_migration_and_CO.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/39773302/jcb.22520-libre.pdf20151107-4768-1o00gty?1446907895=\u0026response-content-disposition=attachment%3B+filename%3DBradykinin_induced_cell_migration_and_CO.pdf\u0026Expires=1732378359\u0026Signature=NaLFgxHRTc~aZIOFH3GivlEuCS-nFWdqDunPLb2zz~Zszq~7BS6TEkKU2VdHFvziR5DcNRcQc9FXkzWqox9MFQxSi-idqyH6KT3Jk-PAdvSrYAOK58qqAd0wdXdri0w1uEnnHWY0jKyZ8DfrmIkwx3ffyHF1VjpqSAU2XaAfcnv7WVY1x7bQojDKzKGY2U1lnu7kLKHIqk~dkA-c~xtFWD3ZRf-KHi398OIDGmeCkBJPQE7DlA5Adoe0Nc4NTovyOoFw5sLkWuLYKV5OKJ2eQpTIB5a8FfeUVkoOamxNAiJMpuMxVSa84baaAb2SVxJIad2BatplUZZ8uZYV0KNs~g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Bradykinin_induced_cell_migration_and_COX_2_production_mediated_by_the_bradykinin_B1_receptor_in_glioma_cells","translated_slug":"","page_count":10,"language":"en","content_type":"Work","owner":{"id":37822776,"first_name":"Kar-lok","middle_initials":null,"last_name":"Wong","page_name":"KarlokWong","domain_name":"independent","created_at":"2015-11-07T06:48:52.756-08:00","display_name":"Kar-lok Wong","url":"https://independent.academia.edu/KarlokWong"},"attachments":[{"id":39773302,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/39773302/thumbnails/1.jpg","file_name":"jcb.22520.pdf20151107-4768-1o00gty","download_url":"https://www.academia.edu/attachments/39773302/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Bradykinin_induced_cell_migration_and_CO.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/39773302/jcb.22520-libre.pdf20151107-4768-1o00gty?1446907895=\u0026response-content-disposition=attachment%3B+filename%3DBradykinin_induced_cell_migration_and_CO.pdf\u0026Expires=1732378359\u0026Signature=NaLFgxHRTc~aZIOFH3GivlEuCS-nFWdqDunPLb2zz~Zszq~7BS6TEkKU2VdHFvziR5DcNRcQc9FXkzWqox9MFQxSi-idqyH6KT3Jk-PAdvSrYAOK58qqAd0wdXdri0w1uEnnHWY0jKyZ8DfrmIkwx3ffyHF1VjpqSAU2XaAfcnv7WVY1x7bQojDKzKGY2U1lnu7kLKHIqk~dkA-c~xtFWD3ZRf-KHi398OIDGmeCkBJPQE7DlA5Adoe0Nc4NTovyOoFw5sLkWuLYKV5OKJ2eQpTIB5a8FfeUVkoOamxNAiJMpuMxVSa84baaAb2SVxJIad2BatplUZZ8uZYV0KNs~g__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":8863,"name":"Cell Migration","url":"https://www.academia.edu/Documents/in/Cell_Migration"},{"id":38831,"name":"Signal Transduction","url":"https://www.academia.edu/Documents/in/Signal_Transduction"},{"id":60915,"name":"Cellular","url":"https://www.academia.edu/Documents/in/Cellular"},{"id":64568,"name":"Humans","url":"https://www.academia.edu/Documents/in/Humans"},{"id":76383,"name":"Glioma","url":"https://www.academia.edu/Documents/in/Glioma"},{"id":99234,"name":"Animals","url":"https://www.academia.edu/Documents/in/Animals"},{"id":375054,"name":"Rats","url":"https://www.academia.edu/Documents/in/Rats"},{"id":1296969,"name":"Molecular and Cellular Biochemistry","url":"https://www.academia.edu/Documents/in/Molecular_and_Cellular_Biochemistry"},{"id":1681026,"name":"Biochemistry and cell biology","url":"https://www.academia.edu/Documents/in/Biochemistry_and_cell_biology"},{"id":2069878,"name":"Bradykinin","url":"https://www.academia.edu/Documents/in/Bradykinin"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906347"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906347/Phloroglucinol_derivative_MCPP_induces_cell_apoptosis_in_human_colon_cancer"><img alt="Research paper thumbnail of Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer" class="work-thumbnail" src="https://attachments.academia-assets.com/42218619/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906347/Phloroglucinol_derivative_MCPP_induces_cell_apoptosis_in_human_colon_cancer">Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer</a></div><div class="wp-workCard_item"><span>Journal of Cellular Biochemistry</span><span>, 2011</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">This study is the first to investigate the anticancer effects of the new phloroglucinol derivativ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2α (eIF-2α), suggesting the induction of ER stress. MCPP also increased GSK3α/β(Tyr270/216) phosphorylation and reduced GSK3α/β(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3α/β activation in mediating the MCPP-induced human colon cancer cell apoptosis.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="6df3aaa569125698c3e5e8d7dad559ad" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":42218619,"asset_id":17906347,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/42218619/download_file?st=MTczMjM3NDc1OSw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906347"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906347"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906347; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906347]").text(description); $(".js-view-count[data-work-id=17906347]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906347; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906347']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906347, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "6df3aaa569125698c3e5e8d7dad559ad" } } $('.js-work-strip[data-work-id=17906347]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906347,"title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon cancer","translated_title":"","metadata":{"abstract":"This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2α (eIF-2α), suggesting the induction of ER stress. MCPP also increased GSK3α/β(Tyr270/216) phosphorylation and reduced GSK3α/β(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3α/β activation in mediating the MCPP-induced human colon cancer cell apoptosis.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Journal of Cellular Biochemistry"},"translated_abstract":"This study is the first to investigate the anticancer effects of the new phloroglucinol derivative (3,6-bis(3-chlorophenylacetyl)phloroglucinol; MCPP) in human colon cancer cells. MCPP induced cell death and antiproliferation in three human colon cancer, HCT-116, SW480, and Caco-2 cells, but not in primary human dermal fibroblast cells. MCPP-induced concentration-dependent apoptotic cell death in colon cancer cells was measured by fluorescence-activated cell sorter (FACS) analysis. Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2α (eIF-2α), suggesting the induction of ER stress. MCPP also increased GSK3α/β(Tyr270/216) phosphorylation and reduced GSK3α/β(Ser21/9) phosphorylation time-dependently. Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis. Treatment of MCPP also increased caspase-7, caspase-9, and caspase-3 activity. The inhibition of caspase activity by z-DEVE-FMK or z-VAD-FMK significantly reduced MCPP-induced apoptosis. Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation. Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3α/β activation in mediating the MCPP-induced human colon cancer cell apoptosis.","internal_url":"https://www.academia.edu/17906347/Phloroglucinol_derivative_MCPP_induces_cell_apoptosis_in_human_colon_cancer","translated_internal_url":"","created_at":"2015-11-07T06:50:11.003-08:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":37822776,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":9010029,"work_id":17906347,"tagging_user_id":37822776,"tagged_user_id":null,"co_author_invite_id":2011212,"email":"y***n@mail.cmu.edu.tw","display_order":0,"name":"Yu-hsin Lin","title":"Phloroglucinol derivative MCPP induces cell apoptosis in human colon 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="17906346"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/17906346/Tetramethylpyrazine_protects_mice_against_thioacetamide_induced_acute_hepatotoxicity"><img alt="Research paper thumbnail of Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/17906346/Tetramethylpyrazine_protects_mice_against_thioacetamide_induced_acute_hepatotoxicity">Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarlokWong">Kar-lok Wong</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://cmu-tw.academia.edu/EdmundSo">Edmund So</a></span></div><div class="wp-workCard_item"><span>Journal of Biomedical Science</span><span>, 2002</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatot...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. TMP appears to act by preventing lipid peroxidation.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="17906346"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="17906346"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 17906346; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=17906346]").text(description); $(".js-view-count[data-work-id=17906346]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 17906346; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='17906346']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 17906346, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=17906346]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":17906346,"title":"Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity","translated_title":"","metadata":{"abstract":"In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. TMP appears to act by preventing lipid peroxidation.","publication_date":{"day":null,"month":null,"year":2002,"errors":{}},"publication_name":"Journal of Biomedical Science"},"translated_abstract":"In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. 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