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[{"id":48914962,"identifier":"Attachment_48914962","shouldShowBulkDownload":false}]; window.loswp.shouldDetectTimezone = true; window.loswp.shouldShowBulkDownload = true; window.loswp.showSignupCaptcha = false window.loswp.willEdgeCache = false; window.loswp.work = {"work":{"id":6329391,"created_at":"2014-03-07T16:31:22.494-08:00","from_world_paper_id":123195021,"updated_at":"2024-11-18T03:00:45.917-08:00","_data":{"grobid_abstract":"Hypoxia-inducible factor-1alpha (HIF-1α) has been considered as a regulator of both prosurvival and prodeath pathways in the nervous system. The present study was designed to elucidate the role of HIF-1α in neonatal hypoxic-ischemic (HI) brain injury. Rice-Vannucci model of neonatal hypoxicischemic brain injury was used in seven-day-old rats, by subjecting unilateral carotid artery ligation followed by 2h of hypoxia (8% O 2 at 37°C). HIF-1α activity was inhibited by 2-methoxyestradiol (2ME2) and enhanced by dimethyloxalylglycine (DMOG). Results showed that 2ME2 exhibited dose-dependent neuroprotection by decreasing infarct volume and reducing brain edema at 48 h post HI. The neuroprotection was lost when 2ME2 was administered 3 h post HI. HIF-1α upregulation by DMOG increased the permeability of the BBB and brain edema compared with HI group. 2ME2 attenuated the increase in HIF-1α and VEGF 24 h after HI. 2ME2 also had a long-term effect of protecting against the loss of brain tissue. The study showed that the early inhibition of HIF-1α acutely after injury provided neuroprotection after neonatal hypoxia-ischemia which was associated with preservation of BBB integrity, attenuation of brain edema, and neuronal death.","publication_date":"2008,,","publication_name":"Neurobiology of Disease","grobid_abstract_attachment_id":"48914962"},"document_type":"paper","pre_hit_view_count_baseline":null,"quality":"high","language":"en","title":"HIF-1α inhibition ameliorates neonatal brain injury in a rat pup hypoxic–ischemic model","broadcastable":true,"draft":null,"has_indexable_attachment":true,"indexable":true}}["work"]; window.loswp.workCoauthors = [9851264]; window.loswp.locale = "en"; window.loswp.countryCode = "SG"; window.loswp.cwvAbTestBucket = ""; window.loswp.designVariant = "ds_vanilla"; window.loswp.fullPageMobileSutdModalVariant = "control"; window.loswp.useOptimizedScribd4genScript = false; window.loswp.appleClientId = 'edu.academia.applesignon';</script><script 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data-landing_url="https://www.academia.edu/6329391/HIF_1%CE%B1_inhibition_ameliorates_neonatal_brain_injury_in_a_rat_pup_hypoxic_ischemic_model" data-login_uri="https://www.academia.edu/registrations/google_one_tap" data-moment_callback="onGoogleOneTapEvent" id="g_id_onload"></div><div class="ds-top-related-works--grid-container"><div class="ds-related-content--container ds-top-related-works--container"><h2 class="ds-related-content--heading">Related papers</h2><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="0" data-entity-id="6329384" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/6329384/HIF_1_alpha_inhibition_ameliorates_neonatal_brain_damage_after_hypoxic_ischemic_injury">HIF-1 alpha inhibition ameliorates neonatal brain damage after hypoxic-ischemic injury</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="9851264" href="https://independent.academia.edu/jadhavvikram">vikram jadhav</a></div><p class="ds-related-work--abstract ds2-5-body-sm">Background Hypoxia-inducible-factor-1alpha (HIF-1α) has been considered as a regulator of both prosurvival and prodeath pathways in the nervous system. This study was designed to elucidate the role of HIF-1α in neonatal hypoxia-ischemia (HI) brain injury. Methods 2-methoxyestradiol (2ME2), a HIF-1α inhibitor, was tested at different dosages (1.5, 15 and 150 mg/kg) and a therapeutic window was tested by administrating 2-methoxyestradiol (15 mg/kg) immediately or 3 hours after the induction of a hypoxic ischemic injury. Infarct size using TTC staining and brain edema were measured at 48 hours post hypoxia-ischemia. Blood-brain barrier (BBB) permeability was examined by IgG staining. Vascular endothelial growth factor (VEGF) and HIF-1α expression and distribution were studied by immunohistochemistry and western blotting analysis. Findings 2ME2 exhibited dose-dependent neuroprotection by decreasing infarct volume and attenuating brain edema. 2ME2 also attenuated BBB disruption, and decreased HIF-1α and vascular endothelial growth factor (VEGF) expression. The neuroprotection, however, was lost when 2ME2 was administered 3 hours after neonatal HI. Conclusion The study shows that the acute inhibition of HIF-1α is neuroprotective in neonatal hypoxic-ischemic injury by preserving BBB integrity and reducing brain edema.</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"HIF-1 alpha inhibition ameliorates neonatal brain damage after hypoxic-ischemic injury","attachmentId":48914844,"attachmentType":"pdf","work_url":"https://www.academia.edu/6329384/HIF_1_alpha_inhibition_ameliorates_neonatal_brain_damage_after_hypoxic_ischemic_injury","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/6329384/HIF_1_alpha_inhibition_ameliorates_neonatal_brain_damage_after_hypoxic_ischemic_injury"><span class="ds2-5-text-link__content">View PDF</span><span class="material-symbols-outlined" style="font-size: 18px" translate="no">chevron_right</span></a></div></div><div class="ds-related-work--container js-wsj-grid-card" data-collection-position="1" data-entity-id="95730430" data-sort-order="default"><a class="ds-related-work--title js-wsj-grid-card-title ds2-5-body-md ds2-5-body-link" href="https://www.academia.edu/95730430/HIF_1%CE%B1_Deficient_Mice_Have_Increased_Brain_Injury_after_Neonatal_Hypoxia_Ischemia">HIF-1α-Deficient Mice Have Increased Brain Injury after Neonatal Hypoxia-Ischemia</a><div class="ds-related-work--metadata"><a class="js-wsj-grid-card-author ds2-5-body-sm ds2-5-body-link" data-author-id="32903116" href="https://independent.academia.edu/DonnaFerriero">Donna Ferriero</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Developmental Neuroscience, 2009</p><p class="ds-related-work--abstract ds2-5-body-sm">Evidence suggests that the activation of the transcription factor hypoxia-inducible factor 1α (HIF-1α) may promote cell survival in hypoxic or ischemic brain. To help understand the role of HIF-1α in neonatal hypoxic-ischemic brain injury, mice with conditional neuron-specific inactivation of HIF-1α underwent hypoxia-ischemia (HI). Mice heterozygous for Cre recombinase under the control of the calcium/calmodulin-dependent kinase II promoter were bred with homozygous ‘floxed’ HIF-1α transgenic mice. The resulting litters produced mice with a forebrain predominant neuronal deletion of HIF-1α (HIF-1αΔ/Δ), as well as littermates without the deletion. In order to verify reduction of HIF-1α at postnatal day 7, HIF-1αΔ/Δ and wild-type mice were exposed to a hypoxic stimulus (8% oxygen) or room air for 1 h, followed by immediate collection of brain cortices for determination of HIF-1α expression. Results of Western blotting of mouse cortices exposed to hypoxia stimulus or room air confirmed...</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"HIF-1α-Deficient Mice Have Increased Brain Injury after Neonatal Hypoxia-Ischemia","attachmentId":97831555,"attachmentType":"pdf","work_url":"https://www.academia.edu/95730430/HIF_1%CE%B1_Deficient_Mice_Have_Increased_Brain_Injury_after_Neonatal_Hypoxia_Ischemia","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-wsj-grid-card-view-pdf" href="https://www.academia.edu/95730430/HIF_1%CE%B1_Deficient_Mice_Have_Increased_Brain_Injury_after_Neonatal_Hypoxia_Ischemia"><span 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data-author-id="47790546" href="https://independent.academia.edu/JamesBrorson">James Brorson</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Experimental Neurology, 2011</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Adaptation to moderate hypoxia protects cortical neurons against ischemia–reperfusion injury and excitotoxicity independently of HIF-1α","attachmentId":89247986,"attachmentType":"pdf","work_url":"https://www.academia.edu/84114849/Adaptation_to_moderate_hypoxia_protects_cortical_neurons_against_ischemia_reperfusion_injury_and_excitotoxicity_independently_of_HIF_1%CE%B1","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline 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data-author-id="32797713" href="https://independent.academia.edu/SchuichiKoizumi">Schuichi Koizumi</a></div><p class="ds-related-work--metadata ds2-5-body-xs">Glia, 2017</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"Hypoxia-independent mechanisms of HIF-1α expression in astrocytes after ischemic preconditioning","attachmentId":87648484,"attachmentType":"pdf","work_url":"https://www.academia.edu/81691697/Hypoxia_independent_mechanisms_of_HIF_1%CE%B1_expression_in_astrocytes_after_ischemic_preconditioning","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-related-work-grid-card-view-pdf" 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class="ds-related-work--metadata ds2-5-body-xs">Brain and Development, 2009</p><div class="ds-related-work--ctas"><button class="ds2-5-text-link ds2-5-text-link--inline js-swp-download-button" data-signup-modal="{"location":"wsj-grid-card-download-pdf-modal","work_title":"The role of hypoxia-inducible transcription factors in the hypoxic neonatal brain","attachmentId":72011461,"attachmentType":"pdf","work_url":"https://www.academia.edu/56806251/The_role_of_hypoxia_inducible_transcription_factors_in_the_hypoxic_neonatal_brain","alternativeTracking":true}"><span class="material-symbols-outlined" style="font-size: 18px" translate="no">download</span><span class="ds2-5-text-link__content">Download free PDF</span></button><a class="ds2-5-text-link ds2-5-text-link--inline js-related-work-grid-card-view-pdf" href="https://www.academia.edu/56806251/The_role_of_hypoxia_inducible_transcription_factors_in_the_hypoxic_neonatal_brain"><span class="ds2-5-text-link__content">View PDF</span><span 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