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inflammation</title> <meta name="description" content="Search results for: inflammation"> <meta name="keywords" content="inflammation"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none navbar-toggler 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id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="inflammation"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 558</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: inflammation</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">558</span> Ancelim: Health System Restoration Protocol for Cancer Patients</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mark%20Berry">Mark Berry</a> </p> <p class="card-text"><strong>Abstract:</strong></p> A number of studies have identified several factors involved in the malignant progression of cancer cells. The Primary modulator in driving inflammation to these transformed cells has been identified as the transcription factor known as nuclear factor-κB. This essential regulator of inflammation and the development of cancer, combined with a microenvironment of inflammation and signaling molecules, plays a major role in the malignant progression of cancer, and this progression is the result of the mutagenic predisposition of persistent substances that combat infection at tumor sites and other areas of chronic inflammation. Inflammation-induced tumors, and their inflammatory cells and regulators may be the primary source of metastasis of tumor cells through angiogenesis. Previous research on cytokines and chemokines, including their downstream targets, has been the focus of the cancer/inflammation connection. The identification of the biological mechanisms of other proteins vital to the inflammation cascade and their interactions are crucial to novel and effective therapeutic protocols for the treatment of inflammation-induced cancers. The Ancelim HSRP Protocol is just such a therapeutic intervention. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ancelim" title="ancelim">ancelim</a>, <a href="https://publications.waset.org/abstracts/search?q=cancer" title=" cancer"> cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=tumor" title=" tumor"> tumor</a> </p> <a href="https://publications.waset.org/abstracts/37512/ancelim-health-system-restoration-protocol-for-cancer-patients" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/37512.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">545</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">557</span> Characterization of Molecular Targets to Mediate Skin Itch and Inflammation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Anita%20J%C3%A4ger">Anita Jäger</a>, <a href="https://publications.waset.org/abstracts/search?q=Andrew%20Salazar"> Andrew Salazar</a>, <a href="https://publications.waset.org/abstracts/search?q=J%C3%B6rg%20von%20Hagen"> Jörg von Hagen</a>, <a href="https://publications.waset.org/abstracts/search?q=Harald%20Kolmar"> Harald Kolmar</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In the treatment of individuals with sensitive and psoriatic skin, several inflammation and itch-related molecular and cellular targets have been identified, but many of these have yet to be characterized. In this study, we present two potential targets in the skin that can be linked to the inflammation and itch cycle. 11ßHSD1 is the enzyme responsible for converting inactive cortisone to active cortisol used to transmit signals downstream. The activation of the receptor NK1R correlates with promoting inflammation and the perception of itch and pain in the skin. In this study, both targets have been investigated based on their involvement in inflammation. The role of both identified targets was characterized based on the secretion of inflammation cytokine- IL6, IL-8, and CCL2, as well as phosphorylation and signaling pathways. It was found that treating skin cells with molecules able to inhibit inflammatory pathways results in the reduction of inflammatory signaling molecules secreted by skin cells and increases their proliferative capacity. Therefore, these molecular targets and their associated pathways show therapeutic potential and can be mitigated via small molecules. This research can be used for further studies in inflammation and itch pathways and can help to treat pathological symptoms. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inflammation" title="inflammation">inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=itch" title=" itch"> itch</a>, <a href="https://publications.waset.org/abstracts/search?q=signaling%20pathway" title=" signaling pathway"> signaling pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=skin" title=" skin"> skin</a> </p> <a href="https://publications.waset.org/abstracts/148393/characterization-of-molecular-targets-to-mediate-skin-itch-and-inflammation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/148393.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">123</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">556</span> Activation of TNF-α from Human Endothelial Cells by Exposure of the Mitochondrial Stress Protein (Hsp60) Secreted from THP-1 Monocytes to High Glucose</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ryan%20D.%20Martinus">Ryan D. Martinus</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Inflammation of the endothelium is an important process leading to diabetic atherosclerosis. However, the molecular mechanisms by which diabetes contributes to endothelial inflammation remain to be established. Using In-vitro cultured Human cells and Hsp60 specific ELISA assays, we show that Hsp60 is not only induced in Human monocyte cells under hyperglycaemic conditions but that the Hsp60 is also secreted from these cells. Furthermore, we also demonstrate that the Hsp60 secreted from these monocyte cells is also able to activate Toll-like receptor-4 (TLR4) from Human endothelial cells. This suggests that a potential link may exist between the hyperglycaemia-induced expression of Hsp60 in monocyte cells and vascular inflammation. Circulating levels of Hsp60 due to mitochondrial stress in diabetes patients could, therefore, be an important modulator of inflammation in endothelial cells and thus contribute to the increased incidences of atherosclerosis in diabetes mellitus. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=mitochondria" title="mitochondria">mitochondria</a>, <a href="https://publications.waset.org/abstracts/search?q=Hsp60" title=" Hsp60"> Hsp60</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=diabetes%20mellitus" title=" diabetes mellitus"> diabetes mellitus</a> </p> <a href="https://publications.waset.org/abstracts/107492/activation-of-tnf-a-from-human-endothelial-cells-by-exposure-of-the-mitochondrial-stress-protein-hsp60-secreted-from-thp-1-monocytes-to-high-glucose" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/107492.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">181</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">555</span> MiRNA Regulation of CXCL12β during Inflammation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Raju%20Ranjha">Raju Ranjha</a>, <a href="https://publications.waset.org/abstracts/search?q=Surbhi%20Aggarwal"> Surbhi Aggarwal</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Inflammation plays an important role in infectious and non-infectious diseases. MiRNA is also reported to play role in inflammation and associated cancers. Chemokine CXCL12 is also known to play role in inflammation and various cancers. CXCL12/CXCR4 chemokine axis was involved in pathogenesis of IBD specially UC. Supplementation of CXCL12 induces homing of dendritic cells to spleen and enhances control of plasmodium parasite in BALB/c mice. We looked at the regulation of CXCL12β by miRNA in UC colitis. Prolonged inflammation of colon in UC patient increases the risk of developing colorectal cancer. We looked at the expression differences of CXCl12β and its targeting miRNA in cancer susceptible area of colon of UC patients. Aim: Aim of this study was to find out the expression regulation of CXCL12β by miRNA in inflammation. Materials and Methods: Biopsy samples and blood samples were collected from UC patients and non-IBD controls. mRNA expression was analyzed using microarray and real-time PCR. CXCL12β targeting miRNA were looked by using online target prediction tools. Expression of CXCL12β in blood samples and cell line supernatant was analyzed using ELISA. miRNA target was validated using dual luciferase assay. Results and conclusion: We found miR-200a regulate the expression of CXCL12β in UC. Expression of CXCL12β was increased in cancer susceptible part of colon and expression of its targeting miRNA was decreased in the same part of colon. miR-200a regulate CXCL12β expression in inflammation and may be an important therapeutic target in inflammation associated cancer. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inflammation" title="inflammation">inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=miRNA" title=" miRNA"> miRNA</a>, <a href="https://publications.waset.org/abstracts/search?q=regulation" title=" regulation"> regulation</a>, <a href="https://publications.waset.org/abstracts/search?q=CXCL12" title=" CXCL12"> CXCL12</a> </p> <a href="https://publications.waset.org/abstracts/69823/mirna-regulation-of-cxcl12v-during-inflammation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/69823.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">278</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">554</span> Phytomolecules Intervening Inflammation in IgA Nephropathy: A Possible Therapeutic Approach</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Rajiv%20Jash">Rajiv Jash</a>, <a href="https://publications.waset.org/abstracts/search?q=Himangshusekhar%20Maji"> Himangshusekhar Maji</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Phytomolecules have long been associated with the effective treatment of various disorders since ages. This study focuses on identifying the immunomodulatory pure molecules isolated from plants, which can be studied for their effect in alleviating IgAN. All the phytomolecules mentioned here have inflammation-reducing properties, and IgAN, being an autoimmune disease, can be a good target of these phytomolecules. Various pathological pathways of IgA nephropathy can be targeted with these phytomolecules, and this study is an effort to find out the rationale behind the choice of the molecules based on their ability to target the effector molecules of those pathological pathways. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=IgAN" title="IgAN">IgAN</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=ESRD" title=" ESRD"> ESRD</a>, <a href="https://publications.waset.org/abstracts/search?q=TGF%CE%B2" title=" TGFβ"> TGFβ</a> </p> <a href="https://publications.waset.org/abstracts/174510/phytomolecules-intervening-inflammation-in-iga-nephropathy-a-possible-therapeutic-approach" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/174510.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">97</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">553</span> Anti-Inflammatory Effect of Myristic Acid through Inhibiting NF-κB and MAPK Signaling Pathways in Lipopolysaccharide-Stimulated RAW 264.7 Macrophage Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Hyun%20Ji%20Hyun">Hyun Ji Hyun</a>, <a href="https://publications.waset.org/abstracts/search?q=Hyo%20Sun%20Suh"> Hyo Sun Suh</a>, <a href="https://publications.waset.org/abstracts/search?q=Min%20Kook%20Kim"> Min Kook Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Yong%20Chan%20Kwon"> Yong Chan Kwon</a>, <a href="https://publications.waset.org/abstracts/search?q=Byung-Mu%20Lee"> Byung-Mu Lee</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Scope: This study is focused on the effect of myristic acid on LPS-induced inflammation in RAW 264.7 macrophage cells. Methods and results: For the experiment, RAW 264.7 mouse macrophage cell line was used. Results showed that treatment with myristic acid can attenuate LPS-induced inflammation. Moreover, myristic acid significantly suppressed expression of inflammatory mediators and down-regulating UVB-induced intracellular ROS generation. Furthermore, myristic acid reduced the expression of NF-κB by inhibiting degradation of IκB-α and ERK, JNK, and p38 pathways by inhibiting phosphorylation in RAW 264.7 macrophage cells. Conclusion: Overall, these data suggest that the myristic acid could reduce LPS-induced inflammation. Acknowledgment: This research was supported by the Ministry of Trade, Industry & Energy(MOTIE), Korea Institute for Advancement of Technology(KIAT) through the Encouragement Program for The Industries of Economic Cooperation Region <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=anti-inflammation" title="anti-inflammation">anti-inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=myristic%20acid" title=" myristic acid"> myristic acid</a>, <a href="https://publications.waset.org/abstracts/search?q=ROS" title=" ROS"> ROS</a>, <a href="https://publications.waset.org/abstracts/search?q=ultraviolet%20light" title=" ultraviolet light"> ultraviolet light</a> </p> <a href="https://publications.waset.org/abstracts/88889/anti-inflammatory-effect-of-myristic-acid-through-inhibiting-nf-kb-and-mapk-signaling-pathways-in-lipopolysaccharide-stimulated-raw-2647-macrophage-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/88889.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">205</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">552</span> Evaluation of Activity of Anacyclus Pyrethrum Methanolic Extract on Acute Inflammation Induced in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dalila%20Bouamra">Dalila Bouamra</a>, <a href="https://publications.waset.org/abstracts/search?q=Chekib%20Arslane%20Baki"> Chekib Arslane Baki</a>, <a href="https://publications.waset.org/abstracts/search?q=Abdelhamid%20Bouchebour"> Abdelhamid Bouchebour</a>, <a href="https://publications.waset.org/abstracts/search?q=Fatiha%20Koussa"> Fatiha Koussa</a>, <a href="https://publications.waset.org/abstracts/search?q=Amel%20Benamara"> Amel Benamara</a>, <a href="https://publications.waset.org/abstracts/search?q=Seoussen%20Kada"> Seoussen Kada</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The activity of methanolic extract from Anacyclus pyrethrum was evaluated using λ-carrageenan 1% induced paw edema in Wistar Albinos rats. The oral administration of 200 mg/kg, 400 mg/kg and 600 mg/kg, body weight of methanolic extract, one hour before induction of inflammation, exerted a significant inhibition effect of 47%, 57% and 62% respectively after 4h λ-carrageenan treatment and highly significant inhibition effect of 57%, 66% and 75% respectively after 8h λ-carrageenan treatment, compared to non treated group (100%) and that treated with aspirin, a standard anti-inflammatory drug. On the other hand, the effect of the plant extract on stomach was macroscopically and microscopically studied. The plant extract has an impact on the loss ratio of granulocytes that have invaded the stomach after a period of inflammation at a dose of 600 mg/kg body weight. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inflammation" title="inflammation">inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=Anacyclus%20pyrethrum" title=" Anacyclus pyrethrum"> Anacyclus pyrethrum</a>, <a href="https://publications.waset.org/abstracts/search?q=gastritis" title=" gastritis"> gastritis</a>, <a href="https://publications.waset.org/abstracts/search?q=Wistar%20Albinos%20rats" title=" Wistar Albinos rats"> Wistar Albinos rats</a> </p> <a href="https://publications.waset.org/abstracts/17054/evaluation-of-activity-of-anacyclus-pyrethrum-methanolic-extract-on-acute-inflammation-induced-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/17054.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">487</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">551</span> Differential Expression of GABA and Its Signaling Components in Ulcerative Colitis and Irritable Bowel Syndrome Pathogenesis</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Surbhi%20Aggarwal">Surbhi Aggarwal</a>, <a href="https://publications.waset.org/abstracts/search?q=Jaishree%20Paul"> Jaishree Paul</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Role of GABA has been implicated in autoimmune diseases like multiple sclerosis, type1 diabetes and rheumatoid arthritis where they modulate the immune response but role in gut inflammation has not been defined. Ulcerative colitis (UC) and diarrhoeal predominant irritable bowel syndrome (IBS-D) both involve inflammation of gastrointestinal tract. UC is a chronic, relapsing and idiopathic inflammation of gut. IBS is a common functional gastrointestinal disorder characterised by abdominal pain, discomfort and alternating bowel habits. Mild inflammation is known to occur in IBS-D. Aim: Aim of this study was to investigate the role of GABA in UC as well as in IBS-D. Materials and methods: Blood and biopsy samples from UC, IBS-D and controls were collected. ELISA was used for measuring level of GABA in serum of UC, IBS-D and controls. RT-PCR analysis was done to determine GABAergic signal system in colon biopsy of UC, IBS-D and controls. RT-PCR was done to check the expression of proinflammatory cytokines. CurveExpert 1.4, Graphpad prism-6 software were used for data analysis. Statistical analysis was done by unpaired, two-way student`s t-test. All sets of data were represented as mean± SEM. A probability level of p < 0.05 was considered statistically significant. Results and conclusion: Significantly decreased level of GABA and altered GABAergic signal system was detected in UC and IBS-D as compared to controls. Significantly increased expression of proinflammatory cytokines was also determined in UC and IBS-D as compared to controls. Hence we conclude that insufficient level of GABA in UC and IBS-D leads to overproduction of proinflammatory cytokines which further contributes to inflammation. GABA may be used as a promising therapeutic target for treatment of gut inflammation or other inflammatory diseases. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=diarrheal%20predominant%20irritable%20bowel%20syndrome" title="diarrheal predominant irritable bowel syndrome">diarrheal predominant irritable bowel syndrome</a>, <a href="https://publications.waset.org/abstracts/search?q=%CE%B3-aminobutyric%20acid%20%28GABA%29" title=" γ-aminobutyric acid (GABA)"> γ-aminobutyric acid (GABA)</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=ulcerative%20colitis" title=" ulcerative colitis"> ulcerative colitis</a> </p> <a href="https://publications.waset.org/abstracts/69853/differential-expression-of-gaba-and-its-signaling-components-in-ulcerative-colitis-and-irritable-bowel-syndrome-pathogenesis" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/69853.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">225</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">550</span> Sulforaphane Attenuates Muscle Inflammation in Dystrophin-Deficient Mdx Mice via Nrf2/HO-1 Signaling Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: Inflammation is widely distributed in patients with Duchenne muscular dystrophy (DMD), and ultimately leads to progressive deterioration of muscle function with the co-effects of chronic muscle damage, oxidative stress, and reduced oxidative capacity. NF-E2-related factor 2 (Nrf2) plays a critical role in defending against inflammation in different tissues via activation of phase II enzymes, heme oxygenase-1 (HO-1). However, whether Nrf2/HO-1 pathway can attenuate muscle inflammation on DMD remains unknown. The purpose of this study was to determine the anti-inflammatory effects of Sulforaphane (SFN) on DMD. Methods: 4-week-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 4 weeks. Gastrocnemius, tibial anterior and triceps brachii muscles were collected for related analysis. Immune cell infiltration in skeletal muscles was analyzed by H&E staining and immuno-histochemistry. Moreover, the expressions of inflammatory cytokines,pro-inflammatory cytokines and Nrf2/HO-1 pathway were detected by western blot, qRT-PCR, immunohistochemistry and immunofluorescence assays. Results: Our results demonstrated that SFN treatment increased the expression of muscle phase II enzymes HO-1 in Nrf2 dependent manner. Inflammation in mdx skeletal muscles was reduced by SFN treatment as indicated by decreased immune cell infiltration and lower expressions of the inflammatory cytokines CD45, pro-inflammatory cytokines tumour necrosis factor-α and interleukin-6 in the skeletal muscles of mdx mice. Conclusions: Collectively, these results show that SFN can ameliorate muscle inflammation in mdx mice by Nrf2/HO-1 pathway, which indicates Nrf2/HO-1 pathway may represent a new therapeutic target for DMD. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=HO-1" title=" HO-1"> HO-1</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a> </p> <a href="https://publications.waset.org/abstracts/19664/sulforaphane-attenuates-muscle-inflammation-in-dystrophin-deficient-mdx-mice-via-nrf2ho-1-signaling-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19664.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">334</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">549</span> Ankaferd Blood Stopper (ABS) Has Protective Effect on Colonic Inflammation: An in Vitro Study in Raw 264.7 and Caco-2 Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Aysegul%20Alyamac">Aysegul Alyamac</a>, <a href="https://publications.waset.org/abstracts/search?q=Sukru%20Gulec"> Sukru Gulec</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Ankaferd Blood Stopper (ABS) is a plant extract used to stop bleeding caused by injuries and surgical interventions. ABS also involved in wound healing of intestinal mucosal damage due to oxidative stress and inflammation. Inflammatory Bowel Disease (IBD) is a common chronic disorder of the gastrointestinal tract that causes abdominal pain, diarrhea, and gastrointestinal bleeding, and increases the risk of colon cancer. Inflammation is an essential factor in the development of IBD. The various studies have been performed about the physiological effects of ABS; however, ABS dependent mechanism on colonic inflammation has not been elucidated. Thus, the protective effect of ABS on colonic inflammation was investigated in this study. The Caco-2 and RAW 264.7 murine macrophage cells were used as a model of in vitro colonic inflammation. RAW 264.7 cells were treated with lipopolysaccharide (LPS) for 12 hours to induce the inflammation, and a conditional medium was obtained. Caco-2 cells were treated with 15 µl/ml ABS for 4 hours, then incubated with conditional medium and the cells also were incubated with 15 µl/ml ABS and conditional medium together for 4 hours. Tumor necrosis factor alpha (TNF-α) protein levels were targeted in testing inflammatory condition and its level was significantly increased (25 fold, p<0.001) compared to the control group by using Enzyme-Linked Immunosorbent Assay (ELISA) method. The COX-2 mRNA level was used as a marker gene to show the possible anti-inflammatory effect of ABS in Caco-2 cells. RAW cells-derived conditional medium significantly (3.3 fold, p<0.001) induced cyclooxygenase-2 (COX-2) mRNA levels in Caco-2 cells. The pretreatment of Caco-2 cells caused a significant decrease (3.3 fold, p<0.001) in COX-2 mRNA levels relative to conditional medium given group. Furthermore, COX-2 mRNA level was significantly reduced (4,7 fold, p<0.001) in ABS and conditional medium treated group. These results suggest that ABS might have an anti-inflammatory effect in vitro. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ankaferd%20blood%20stopper" title="Ankaferd blood stopper">Ankaferd blood stopper</a>, <a href="https://publications.waset.org/abstracts/search?q=CaCo-2" title=" CaCo-2"> CaCo-2</a>, <a href="https://publications.waset.org/abstracts/search?q=colonic%20inflammation" title=" colonic inflammation"> colonic inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=RAW%20264.7" title=" RAW 264.7"> RAW 264.7</a> </p> <a href="https://publications.waset.org/abstracts/121210/ankaferd-blood-stopper-abs-has-protective-effect-on-colonic-inflammation-an-in-vitro-study-in-raw-2647-and-caco-2-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/121210.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">146</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">548</span> Detecting Rat’s Kidney Inflammation Using Real Time Photoacoustic Tomography</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=M.%20Y.%20Lee">M. Y. Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=D.%20H.%20Shin"> D. H. Shin</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20H.%20Park"> S. H. Park</a>, <a href="https://publications.waset.org/abstracts/search?q=W.C.%20Ham"> W.C. Ham</a>, <a href="https://publications.waset.org/abstracts/search?q=S.K.%20Ko"> S.K. Ko</a>, <a href="https://publications.waset.org/abstracts/search?q=C.%20G.%20Song"> C. G. Song </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Photoacoustic Tomography (PAT) is a promising medical imaging modality that combines optical imaging contrast with the spatial resolution of ultrasound imaging. It can also distinguish the changes in biological features. But, real-time PAT system should be confirmed due to photoacoustic effect for tissue. Thus, we have developed a real-time PAT system using a custom-developed data acquisition board and ultrasound linear probe. To evaluate performance of our system, phantom test was performed. As a result of those experiments, the system showed satisfactory performance and its usefulness has been confirmed. We monitored the degradation of inflammation which induced on the rat’s kidney using real-time PAT. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=photoacoustic%20tomography" title="photoacoustic tomography">photoacoustic tomography</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation%20detection" title=" inflammation detection"> inflammation detection</a>, <a href="https://publications.waset.org/abstracts/search?q=rat" title=" rat"> rat</a>, <a href="https://publications.waset.org/abstracts/search?q=kidney" title=" kidney"> kidney</a>, <a href="https://publications.waset.org/abstracts/search?q=contrast%20agent" title=" contrast agent"> contrast agent</a>, <a href="https://publications.waset.org/abstracts/search?q=ultrasound" title=" ultrasound"> ultrasound</a> </p> <a href="https://publications.waset.org/abstracts/71172/detecting-rats-kidney-inflammation-using-real-time-photoacoustic-tomography" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/71172.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">457</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">547</span> Preclinical Studying of Stable Fe-Citrate Effect on 68Ga-Citrate Tissue Distribution</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=A.%20S.%20Lunev">A. S. Lunev</a>, <a href="https://publications.waset.org/abstracts/search?q=A.%20A.%20Larenkov"> A. A. Larenkov</a>, <a href="https://publications.waset.org/abstracts/search?q=O.%20E.%20Klementyeva"> O. E. Klementyeva</a>, <a href="https://publications.waset.org/abstracts/search?q=G.%20E.%20Kodina"> G. E. Kodina</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background and aims: 68Ga-citrate is one of prospective radiopharmaceutical for PET-imaging of inflammation and infection. 68Ga-citrate is 67Ga-citrate analogue using since 1970s for SPECT-imaging. There's known rebinding reaction occurs past Ga-citrate injection and gallium (similar iron Fe3+) binds with blood transferrin. Then radiolabeled protein complex is delivered to pathological foci (inflammation/infection sites). But excessive gallium bindings with transferrin are cause of slow blood clearance, long accumulation time in foci (24-72 h) and exception of application possibility of the short-lived gallium-68 (T½ = 68 min). Injection of additional chemical agents (e.g. Fe3+ compounds) competing with radioactive gallium to the blood transferrin joining (blocking of its metal binding capacity) is one of the ways to solve formulated problem. This phenomenon can be used for correction of 68Ga-citrate pharmacokinetics for increasing of the blood clearance and accumulation in foci. The aim of real studying is research of effect of stable Fe-citrate on 68Ga-citrate tissue distribution. Materials and methods: 68Ga-citrate without/with extra injection of stable Fe-citrate (III) was injected nonlinear mice with inflammation models (aseptic soft tissue inflammation, lung infection, osteomyelitis). PET/X-RAY Genisys4 (Sofie Bioscience, USA) was used for non-invasive PET imaging (for 30, 60, 120 min past injection 68Ga-citrate) with subsequent reconstruction of imaging and their analysis (value of clearance, distribution volume). Scanning time is 10 min. Results and conclusions: I. v. injection of stable Fe-citrate blocks the metal-binding capability of transferrin serum and allows decreasing gallium-68 radioactivity in blood significantly and increasing accumulation in inflammation (3-5 time). It allows receiving more informative PET-images of inflammation early (for 30-60 min after injection). Pharmacokinetic parameters prove it. Noted there is no statistically significant difference between 68Ga-citrate accumulation for different inflammation model because PET imaging is indication of pathological processes and is not their identification. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=68Ga-citrate" title="68Ga-citrate">68Ga-citrate</a>, <a href="https://publications.waset.org/abstracts/search?q=Fe-citrate" title=" Fe-citrate"> Fe-citrate</a>, <a href="https://publications.waset.org/abstracts/search?q=PET%20imaging" title=" PET imaging"> PET imaging</a>, <a href="https://publications.waset.org/abstracts/search?q=mice" title=" mice"> mice</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=infection" title=" infection"> infection</a> </p> <a href="https://publications.waset.org/abstracts/34962/preclinical-studying-of-stable-fe-citrate-effect-on-68ga-citrate-tissue-distribution" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/34962.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">488</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">546</span> Antioxidant Potential of Pomegranate Rind Extract Attenuates Pain, Inflammation and Bone Damage in Experimental Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ritu%20Karwasra">Ritu Karwasra</a>, <a href="https://publications.waset.org/abstracts/search?q=Surender%20Singh"> Surender Singh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Inflammation is an important physiological response of the body’s self-defense system that helps in eliminating and protecting organism from harmful stimuli and in tissue repair. It is a highly regulated protective response which helps in eliminating the initial cause of cell injury, and initiates the process of repair. The present study was designed to evaluate the ameliorative effect of pomegranate rind extract on pain and inflammation. Hydroalcoholic standardized rind extract of pomegranate at doses 50, 100 and 200 mg/kg and indomethacin (3 mg/kg) was tested against eddy’s hot plate induced thermal algesia, carrageenan (acute inflammation) and Complete Freund’s Adjuvant (chronic inflammation) induced models in Wistar rats. Parameters analyzed were inhibition of paw edema, measurement of joint diameter, levels of GSH, TBARS, SOD, TNF-α, radiographic imaging, tissue histology and synovial expression of pro-inflammatory cytokine receptor (TNF-R1). Radiological and light microscopical analysis were carried out to find out the bone damage in CFA-induced chronic inflammatory model. Findings of the present study revealed that pomegranate rind extract at a dose of 200 mg/kg caused a significant (p<0.05) reduction in paw swelling in both the inflammatory models. Nociceptive threshold was also significantly (p<0.05) improved. Immunohistochemical analysis of TNF-R1 in CFA-induced group showed elevated level, whereas reduction in level of TNF-R1 was observed in pomegranate (200 mg/kg). Henceforth, we might say that pomegranate produced a dose-dependent reduction in inflammation and pain along with the reduction in levels of oxidative stress markers and tissue histology, and the effect was found to be comparable to that of indomethacin. Thus, it can be concluded that pomegranate is a potential therapeutic target in the pathogenesis of inflammation and pain, and punicalagin is the major constituents found in rind extract might be responsible for the activity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=carrageenan" title="carrageenan">carrageenan</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=nociceptive-threshold" title=" nociceptive-threshold"> nociceptive-threshold</a>, <a href="https://publications.waset.org/abstracts/search?q=pomegranate" title=" pomegranate"> pomegranate</a>, <a href="https://publications.waset.org/abstracts/search?q=histopathology" title=" histopathology"> histopathology</a> </p> <a href="https://publications.waset.org/abstracts/53481/antioxidant-potential-of-pomegranate-rind-extract-attenuates-pain-inflammation-and-bone-damage-in-experimental-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/53481.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">219</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">545</span> Deniplant Nutraceuticals for Endometriosis Pain</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Gheorghe%20Giurgiu">Gheorghe Giurgiu</a>, <a href="https://publications.waset.org/abstracts/search?q=Manole%20Cojocaru"> Manole Cojocaru</a>, <a href="https://publications.waset.org/abstracts/search?q=Mihnea%20Andrei%20Nicodin"> Mihnea Andrei Nicodin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Inflammation has the main role in the progression of endometriosis. The mechanisms by which endometriosis induces a chronic pain state remain poorly understood. Unfortunately, there is no known cure for endometriosis. But you can manage it with medication and at-home treatments. Some findings have highlighted the main role of inflammation in endometriosis by acting on proliferation, apoptosis, and angiogenesis. The introduction of new agents can be effective in improving the condition of patients; for example, plants are promising sources of bioactive natural components. Objectives: These natural compounds could be interesting strategies in therapy. While there is no absolute cure for this condition, some home remedies can relieve the pain and discomfort it brings. The purpose of this study is to summarize the potential action of Deniplant nutraceuticals in endometriosis by acting on inflammation. Materials and Methods: The primary symptoms of endometriosis are pelvic pain and infertility. The use of Deniplant nutraceuticals could be interesting in disease management for women. Results: Treating pain-related aspects of endometriosis would contribute to the improvement of mental health and daytime function. Because the microbiome can influence inflammation, new therapies can develop through its natural modulation. There are other options, including natural remedies, herbs like cinnamon twigs or licorice root, or supplements such as thiamine, magnesium, or omega-3 fatty acids. Conclusion: Deniplant nutraceuticals can downregulate inflammation in endometriosis. Nevertheless, the limited number of studies focusing on the different interactions of Deniplant nutraceuticals in endometriosis restricts its clear and immediate use in a therapeutic strategy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=endometriosis" title="endometriosis">endometriosis</a>, <a href="https://publications.waset.org/abstracts/search?q=diet" title=" diet"> diet</a>, <a href="https://publications.waset.org/abstracts/search?q=Deniplant%20nutraceuticals" title=" Deniplant nutraceuticals"> Deniplant nutraceuticals</a>, <a href="https://publications.waset.org/abstracts/search?q=pain" title=" pain"> pain</a> </p> <a href="https://publications.waset.org/abstracts/145850/deniplant-nutraceuticals-for-endometriosis-pain" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/145850.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">76</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">544</span> Safety Study of Intravenously Administered Human Cord Blood Stem Cells in the Treatment of Symptoms Related to Chronic Inflammation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Brian%20M.%20Mehling">Brian M. Mehling</a>, <a href="https://publications.waset.org/abstracts/search?q=Louis%20Quartararo"> Louis Quartararo</a>, <a href="https://publications.waset.org/abstracts/search?q=Marine%20Manvelyan"> Marine Manvelyan</a>, <a href="https://publications.waset.org/abstracts/search?q=Paul%20Wang"> Paul Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dong-Cheng%20Wu"> Dong-Cheng Wu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Numerous investigations suggest that Mesenchymal Stem Cells (MSCs) in general represent a valuable tool for therapy of symptoms related to chronic inflammatory diseases. Blue Horizon Stem Cell Therapy Program is a leading provider of adult and children’s stem cell therapies. Uniquely we have safely and efficiently treated more than 600 patients with documenting each procedure. The purpose of our study is primarily to monitor the immune response in order to validate the safety of intravenous infusion of human umbilical cord blood derived MSCs (UC-MSCs), and secondly, to evaluate effects on biomarkers associated with chronic inflammation. Nine patients were treated for conditions associated with chronic inflammation and for the purpose of anti-aging. They have been given one intravenous infusion of UC-MSCs. Our study of blood test markers of 9 patients with chronic inflammation before and within three months after MSCs treatment demonstrates that there is no significant changes and MSCs treatment was safe for the patients. Analysis of different indicators of chronic inflammation and aging included in initial, 24-hours, two weeks and three months protocols showed that stem cell treatment was safe for the patients; there were no adverse reactions. Moreover data from follow up protocols demonstrates significant improvement in energy level, hair, nails growth and skin conditions. Intravenously administered UC-MSCs were safe and effective in the improvement of symptoms related to chronic inflammation. Further close monitoring and inclusion of more patients are necessary to fully characterize the advantages of UC-MSCs application in treatment of symptoms related to chronic inflammation. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=chronic%20inflammatory%20diseases" title="chronic inflammatory diseases">chronic inflammatory diseases</a>, <a href="https://publications.waset.org/abstracts/search?q=intravenous%20infusion" title=" intravenous infusion"> intravenous infusion</a>, <a href="https://publications.waset.org/abstracts/search?q=stem%20cell%20therapy" title=" stem cell therapy"> stem cell therapy</a>, <a href="https://publications.waset.org/abstracts/search?q=umbilical%20cord%20blood%20derived%20mesenchymal%20stem%20cells%20%28UC-MSCs%29" title=" umbilical cord blood derived mesenchymal stem cells (UC-MSCs)"> umbilical cord blood derived mesenchymal stem cells (UC-MSCs)</a> </p> <a href="https://publications.waset.org/abstracts/32420/safety-study-of-intravenously-administered-human-cord-blood-stem-cells-in-the-treatment-of-symptoms-related-to-chronic-inflammation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/32420.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">433</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">543</span> YPFS Attenuating TH2 Cell-Mediated Allergic Inflammation by Regulating the TSLP Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Xi%20Yu">Xi Yu</a>, <a href="https://publications.waset.org/abstracts/search?q=Lili%20Gu"> Lili Gu</a>, <a href="https://publications.waset.org/abstracts/search?q=Huizhu%20Wang"> Huizhu Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Xiao%20Wei"> Xiao Wei</a>, <a href="https://publications.waset.org/abstracts/search?q=Dandan%20Sheng"> Dandan Sheng</a>, <a href="https://publications.waset.org/abstracts/search?q=Xiaoyan%20Jiang"> Xiaoyan Jiang</a>, <a href="https://publications.waset.org/abstracts/search?q=Min%20Hong"> Min Hong </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: Hypersensitivity disease is difficult to cure completely because of its recurrence, yupingfengsan (YPFS) is used to treat the diseases with the advantage of reducing the recurrence,but the precise mechanism is not clear. Previous studies of our laboratory have shown that the extract of YPFS can inhibit Th2-type allergic contact dermatitis(ACD) induced by FITC.Besides, thymic stromal lymphopoietin(TSLP) have been proved to be a master switch for allergic inflammation. Based on these studies, we want to establish a mouse model of TSLP production based on Th2 cell-mediated allergic inflammation to explore the regulating mechanisms of YPFS on TSLP in Th2 cell-mediated allergic inflammation. Methods: Th2-type ACD mouse model: The mice were topically sensitized on the abdomens (induction phase) and elicited on its ears skin 6 day later (excitation phase) with FITC solution, and the ear swelling was measured to evaluate the allergic inflammation；A mouse model of TSLP production based on Th2 cell-mediated allergic inflammation (TSLP production model): the skin of the ear was sensitized on two consecutive days with FITC solution causing the production of TSLP；Mice were treated with YPFS extract，ELISA、Real-time PCR and Western-blotting were using to examine the mRNA and protein levels of TSLP\TSLPR and TLRs ect. Results: YPFS extract can attenuates Th2-type allergic inflammatory in mice；in TSLP production model, YPFS can inhibit the expression of TSLP、 TSLPR、TLRs and MyD88, So we deduce the possible mechanisms of YPFS to play a role of intervention is through TLRs- MyD88 dependent and independent pathway to reduce TSLP production. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=YPFS" title="YPFS">YPFS</a>, <a href="https://publications.waset.org/abstracts/search?q=TSLP" title=" TSLP"> TSLP</a>, <a href="https://publications.waset.org/abstracts/search?q=TLRs" title=" TLRs"> TLRs</a>, <a href="https://publications.waset.org/abstracts/search?q=Th2-type%20allergic%20contact%20dermatitis" title=" Th2-type allergic contact dermatitis"> Th2-type allergic contact dermatitis</a> </p> <a href="https://publications.waset.org/abstracts/3044/ypfs-attenuating-th2-cell-mediated-allergic-inflammation-by-regulating-the-tslp-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/3044.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">422</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">542</span> The Anti-Inflammatory Effects of Nanodiamond Particles and Lipoic Acid on Rats' Cardiovascular System</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Beata%20Skibska">Beata Skibska</a>, <a href="https://publications.waset.org/abstracts/search?q=Andrzej%20Stanczak"> Andrzej Stanczak</a>, <a href="https://publications.waset.org/abstracts/search?q=Agnieszka%20Skibska"> Agnieszka Skibska</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Nanodiamond (ND) is a carbon nanomaterial that has high biocompatibility, and it has a very positive effect on a number of biochemical processes. NDs have great potential in treating multiple inflammation-associated diseases. The purpose of this study was to investigate the anti-inflammatory effect of nanodiamonds and lipoic acid (LA) (as antioxidants) on rats' cardiovascular systems after lipopolysaccharide (LPS) administration. Animal experiments enabled the determination of how nanodiamonds act when applied independently or in combination with lipoic acid. The effect of NDs and LA on C-reactive protein (CRP) levels and heart edema was evaluated. NDs and LA administered after LPS administration attenuated heart edema and significantly decreased the CRP level. The results suggest that NDs and LA play an important role in LPS-induced inflammation in the heart. NDs find new applications in modern biomedical science and biotechnologies. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=nanodiamonds" title="nanodiamonds">nanodiamonds</a>, <a href="https://publications.waset.org/abstracts/search?q=lipoic%20acid" title=" lipoic acid"> lipoic acid</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=cardiovascular%20system" title=" cardiovascular system"> cardiovascular system</a> </p> <a href="https://publications.waset.org/abstracts/165206/the-anti-inflammatory-effects-of-nanodiamond-particles-and-lipoic-acid-on-rats-cardiovascular-system" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/165206.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">86</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">541</span> Nanoparticles Activated Inflammasome Lead to Airway Hyperresponsiveness and Inflammation in a Mouse Model of Asthma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Pureun-Haneul%20Lee">Pureun-Haneul Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Byeong-Gon%20Kim"> Byeong-Gon Kim</a>, <a href="https://publications.waset.org/abstracts/search?q=Sun-Hye%20Lee"> Sun-Hye Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=An-Soo%20Jang"> An-Soo Jang</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Nanoparticles may pose adverse health effects due to particulate matter inhalation. Nanoparticle exposure induces cell and tissue damage, causing local and systemic inflammatory responses. The inflammasome is a major regulator of inflammation through its activation of pro-caspase-1, which cleaves pro-interleukin-1β (IL-1β) into its mature form and may signal acute and chronic immune responses to nanoparticles. Objective: The aim of the study was to identify whether nanoparticles exaggerates inflammasome pathway leading to airway inflammation and hyperresponsiveness in an allergic mice model of asthma. Methods: Mice were treated with saline (sham), OVA-sensitized and challenged (OVA), or titanium dioxide nanoparticles. Lung interleukin 1 beta (IL-1β), interleukin 18 (IL-18), NACHT, LRR and PYD domains-containing protein 3 (NLRP3) and caspase-1 levels were assessed with Western Blot. Caspase-1 was checked by immunohistochemical staining. Reactive oxygen species were measured for the marker 8-isoprostane and carbonyl by ELISA. Results: Airway inflammation and hyperresponsiveness increased in OVA-sensitized/challenged mice and these responses were exaggerated by TiO2 nanoparticles exposure. TiO2 nanoparticles treatment increased IL-1β and IL-18 protein expression in OVA-sensitized/challenged mice. TiO2 nanoparticles augmented the expression of NLRP3 and caspase-1 leading to the formation of an active caspase-1 in the lung. Lung caspase-1 expression was increased in OVA-sensitized/challenged mice and these responses were exaggerated by TiO2 nanoparticles exposure. Reactive oxygen species was increased in OVA-sensitized/challenged mice and in OVA-sensitized/challenged plus TiO2 exposed mice. Conclusion: Our data demonstrate that inflammasome pathway activates in asthmatic lungs following nanoparticles exposure, suggesting that targeting the inflammasome may help control nanoparticles-induced airway inflammation and responsiveness. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bronchial%20asthma" title="bronchial asthma">bronchial asthma</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammasome" title=" inflammasome"> inflammasome</a>, <a href="https://publications.waset.org/abstracts/search?q=nanoparticles" title=" nanoparticles"> nanoparticles</a> </p> <a href="https://publications.waset.org/abstracts/44817/nanoparticles-activated-inflammasome-lead-to-airway-hyperresponsiveness-and-inflammation-in-a-mouse-model-of-asthma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/44817.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">375</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">540</span> Protective Effect of Bexarotene, a Selective RXRα Agonist, against Hypotension Associated with Inflammation and Tissue Injury Linked to Decreased Circulating iNOS Levels in A Rat Model of Septic Shock</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Bahar%20Tunctan">Bahar Tunctan</a>, <a href="https://publications.waset.org/abstracts/search?q=Sefika%20Pinar%20Kucukkavruk"> Sefika Pinar Kucukkavruk</a>, <a href="https://publications.waset.org/abstracts/search?q=Meryem%20Temiz-Resitoglu"> Meryem Temiz-Resitoglu</a>, <a href="https://publications.waset.org/abstracts/search?q=Demet%20Sinem%20Guden"> Demet Sinem Guden</a>, <a href="https://publications.waset.org/abstracts/search?q=Ayse%20Nihal%20Sari"> Ayse Nihal Sari</a>, <a href="https://publications.waset.org/abstracts/search?q=Seyhan%20Sahan-Firat"> Seyhan Sahan-Firat</a> </p> <p class="card-text"><strong>Abstract:</strong></p> We hypothesized that rexinoids such as bexarotene, a selective retinoid X receptor α (RXRα) agonist, may be beneficial for preventing mortality due to inflammation associated with increased expression/activity of inducible nitric oxide synthase (iNOS) induced by lipopolysaccharide (LPS). Therefore, we investigated effects of bexarotene on the changes in circulating protein levels of iNOS (an index for systemic iNOS expression), myeloperoxidase (MPO) (an index for systemic inflammation), and lactate dehydrogenase (LDH) (an index for systemic tissue injury) in LPS-induced systemic inflammation model resulting in septic shock in rats. Rats were injected with saline (4 ml/kg; i.p.), LPS (10 mg/kg; i.p.), dimethylsulphoxide (4 ml/kg, 0.1%; s.c.) at time 0. Mean arterial blood pressure and heart rate were measured using a tail-cuff device. Bexarotene (0.03, 0.1, 0.3, and 1 mg/kg; s.c.) was administered to separate groups of rats 1 h after injection of saline or LPS. The rats were sacrificed 4 h after saline or LPS injection and blood was collected for measurement of serum iNOS, MPO, and LDH protein levels. Blood pressure decreased by 31 mmHg and heart rate increased by 63 bpm in the LPS-treated rats. Bexarotene at 0.3 and 1 mg/kg doses caused 20% mortality 4 h after LPS injection. In the LPS-treated rats, serum iNOS, MPO, and LDH protein levels were increased. Bexarotene only at 0.1 mg/kg dose prevented the LPS-induced hypotension and increased in iNOS, MPO, and LDH protein levels. These data are consistent with the view that a decrease in systemic iNOS levels contributes to the beneficial effect of bexarotene to prevent the hypotension associated with inflammation and tissue injury during rat endotoxemia. [This work was financially supported by The Scientific and Technological Research Council of Turkey (SBAG-109S121)]. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bexarotene" title="bexarotene">bexarotene</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=iNOS" title=" iNOS"> iNOS</a>, <a href="https://publications.waset.org/abstracts/search?q=lipopolisaccharide" title=" lipopolisaccharide"> lipopolisaccharide</a>, <a href="https://publications.waset.org/abstracts/search?q=RXRa" title=" RXRa"> RXRa</a> </p> <a href="https://publications.waset.org/abstracts/68276/protective-effect-of-bexarotene-a-selective-rxra-agonist-against-hypotension-associated-with-inflammation-and-tissue-injury-linked-to-decreased-circulating-inos-levels-in-a-rat-model-of-septic-shock" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/68276.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">318</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">539</span> Synthesis and Anti-Inflammatory Activity of Pyrazol-3-yl Thiazole 4-Carboxylic Acid Derivatives Targeting Enzyme in the Leukotriene Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Shweta%20Sinha">Shweta Sinha</a>, <a href="https://publications.waset.org/abstracts/search?q=Mukesh%20Doble"> Mukesh Doble</a>, <a href="https://publications.waset.org/abstracts/search?q=Manju%20S.%20L."> Manju S. L.</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Pyrazole scaffold is an important group of compound in heterocyclic chemistry and is found to possess numerous uses in chemistry. Pyrazole derivatives are also known to possess important biological activities including antitumor, antimicrobial, antiviral, antifungal, anticancer and anti-inflammatory. Inflammation is associated with pain, allergy and asthma. Leukotrienes are mediators of various inflammatory and allergic disorders. 5-Lipoxygenase (5-LOX) is an important enzyme involved in the biosynthesis of leukotrienes and metabolism of arachidonic acid (AA) and thus targeted for anti-inflammation. In vitro inhibitory activity of pyrazol-3-yl thiazole 4-carboxylic acid derivatives is tested against enzyme 5-LOX. Most of these compounds exhibit good inhibitory activity against this enzyme. Binding mode study of these compounds is determined by computational tool. Further experiments are being done to understand the mechanism of action of these compounds in inhibiting this enzyme. To conclude, these compounds appear to be a promising target in drug design against 5-LOX. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inflammation" title="inflammation">inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=inhibition" title=" inhibition"> inhibition</a>, <a href="https://publications.waset.org/abstracts/search?q=5-lipoxygenase" title=" 5-lipoxygenase"> 5-lipoxygenase</a>, <a href="https://publications.waset.org/abstracts/search?q=pyrazole" title=" pyrazole"> pyrazole</a> </p> <a href="https://publications.waset.org/abstracts/71661/synthesis-and-anti-inflammatory-activity-of-pyrazol-3-yl-thiazole-4-carboxylic-acid-derivatives-targeting-enzyme-in-the-leukotriene-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/71661.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">244</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">538</span> The Relation Between Oxidative Stress, Inflammation, and Neopterin in the Paraquat-Induced Lung Toxicity</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=M.%20Toygar">M. Toygar</a>, <a href="https://publications.waset.org/abstracts/search?q=I.%20Aydin"> I. Aydin</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Agilli"> M. Agilli</a>, <a href="https://publications.waset.org/abstracts/search?q=F.%20N.%20Aydin"> F. N. Aydin</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Oztosun"> M. Oztosun</a>, <a href="https://publications.waset.org/abstracts/search?q=H.%20Gul"> H. Gul</a>, <a href="https://publications.waset.org/abstracts/search?q=E.%20Macit"> E. Macit</a>, <a href="https://publications.waset.org/abstracts/search?q=Y.%20Karslioglu"> Y. Karslioglu</a>, <a href="https://publications.waset.org/abstracts/search?q=T.%20Topal"> T. Topal</a>, <a href="https://publications.waset.org/abstracts/search?q=B.%20Uysal"> B. Uysal</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Honca"> M. Honca</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Paraquat (PQ) is a well-known quaternary nitrogen herbicide. The major target organ in PQ poisoning is the lung. Reactive oxygen species (ROS) and inflammation play a crucial role in the development of PQ-induced pulmonary injury. Neopterin is synthesized in macrophage by interferon g and other cytokines. We aimed to evaluate the utility of neopterin as a diagnostic marker in PQ-induced lung toxicity. Sprague Dawley rats were randomly divided into two groups (sham and PQ), administered intraperitoneally 1 mL saline and PQ (15 mg/kg/mL) respectively. Blood samples and lungs were collected for analyses. Lung injury and fibrosis were seen in the PQ group. Serum total antioxidant capacity, lactate dehydrogenase (LDH), and lung transforming growth factor-1 (TGF-1) levels were significantly higher than the sham group (in all, p< 0.001). In addition, in the PQ group, serum neopterin and lung malondialdehyde (MDA) levels were also significantly higher than the sham group (in all, p 1/4 0.001). Serum neopterin levels were correlated with LDH activities, lung MDA, lung TGF-1 levels, and the degree of lung injury. These findings demonstrated that oxidative stress, reduction of antioxidant capacity, and inflammation play a crucial role in the PQ-induced lung injury. Elevated serum neopterin levels may be a prognostic parameter to determine extends of PQ-induced lung toxicity. Further studies may be performed to clarify the role of neopterin by different doses of PQ. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=paraquat" title="paraquat">paraquat</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=neopterin" title=" neopterin"> neopterin</a>, <a href="https://publications.waset.org/abstracts/search?q=lung%20toxicity" title=" lung toxicity"> lung toxicity</a> </p> <a href="https://publications.waset.org/abstracts/13543/the-relation-between-oxidative-stress-inflammation-and-neopterin-in-the-paraquat-induced-lung-toxicity" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/13543.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">383</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">537</span> Anti-Inflammatory Effect of Carvedilol 1% Ointment in Topical Application to the Animal Model</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Berina%20Pilipovi%C4%87">Berina Pilipović</a>, <a href="https://publications.waset.org/abstracts/search?q=Sa%C5%A1a%20Pilipovi%C4%87"> Saša Pilipović</a>, <a href="https://publications.waset.org/abstracts/search?q=Maja%20Pa%C5%A1i%C4%87-Kulenovi%C4%87"> Maja Pašić-Kulenović</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Inflammation is the body's response to impaired homeostasis caused by infection, injury or trauma resulting in systemic and local effects. Inflammation causes the body's response to injury and is characterized by a series of events including inflammatory response, response to pain receptors and the recovery process. Inflammation can be acute and chronic. The inflammatory response is described in three different phases. Free radical is an atom or molecule that has the unpaired electron and is therefore generally very reactive chemical species. Biologically important example of reaction with free radicals is called Lipid peroxidation (LP). Lipid peroxidation reactions occur in biological membranes, and if at the outset is not stopped with the action of antioxidants, it will bring damage to the membrane, which results in partial or complete loss of their physiological functions. Calcium antagonists and beta-adrenergic receptor antagonists are known drugs, and for many years and widely used in the treatment of cardiovascular diseases. Some of these compounds also show antioxidant activity. The mechanism of antioxidant activities of calcium antagonists and beta-blockers is unknown, since their structure varies widely. This research investigated the possible local anti-inflammatory activity of ointments containing 1% carvedilol in the white petrolatum USP. Ear inflammation was induced by 3% croton oil acetone solution, in quantity of 10 µl on both mouse ears. Albino Swiss mouse (n = 8) are treated with 2.5 mg/ear ointment, and control group was treated on the same way as previous with hydrocortisone 1% ointment (2.5 mg/ear). The other ear of the same animal was used as control one. Ointments were administered once per day, on the left ear. After treatment, ears were observed for three days. After three days, we measured mass (mg) of 6 mm ear punch of treated and controlled ears. The results of testing anti-inflammatory effects of ointments with carvedilol in the mouse ear model show stronger observed effect than ointment with 1% hydrocortisone in the same basis. Identical results were confirmed by the difference between the mass of 6 mm ears punch. The results were also confirmed by histological examination. Ointments with carvedilol showed significant reduction of the inflammation process caused by croton oil on the mouse inflammation model. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=antioxidant" title="antioxidant">antioxidant</a>, <a href="https://publications.waset.org/abstracts/search?q=carvedilol" title=" carvedilol"> carvedilol</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=mouse%20ear" title=" mouse ear"> mouse ear</a> </p> <a href="https://publications.waset.org/abstracts/68212/anti-inflammatory-effect-of-carvedilol-1-ointment-in-topical-application-to-the-animal-model" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/68212.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">234</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">536</span> Design, Synthesis, and Evaluation of Small Peptides for Managing Inflammation: Inhibition to Substrate Approach</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Palwinder%20Singh">Palwinder Singh</a>, <a href="https://publications.waset.org/abstracts/search?q=Baljit%20Kaur"> Baljit Kaur</a>, <a href="https://publications.waset.org/abstracts/search?q=Sukhmeet%20Kaur"> Sukhmeet Kaur</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Amongst a library of rationally designed small peptides, (H)Gly-Gly-Phe-Leu(OMe) was identified, reducing prostaglandin production of COX-2 with IC50 60 nM vs. 6000 nM for COX-1. The 5 mg Kg-1 dose of this compound rescued albino mice by 80% from capsaicin-induced paw licking and recovered it by 60% from carrageenan-induced inflammation. The mode of action of the compound for targeting COX-2, iNOS, and VGSC was investigated by using substances P, L-arginine, and veratrine, respectively, as the biomarkers. The interactions of the potent compound with COX-2 were supported by the isothermal calorimetry experiments showing Ka 6.10±1.10x104 mol-1 and ΔG -100.3 k J mol-1 in comparison to Ka 0.41x103 ±0.09 mol-1 and ΔG -19.2±0.06 k J mol-1 for COX-1. This compound did not show toxicity up to 2000 mg Kg-1 dose. Furthermore, beyond the conventional mode of working with anti-inflammatory agents through enzyme inhibition, COX-2 was provided with a peptide-based alternate substrate. Proline-centered pentapeptide iso-conformational to arachidonic acid exhibited appreciable selectivity for COX-2 overcoming acetic acid and formalin-induced pain in rats to almost 80% and was treated as a substrate by the enzyme. Hence, we suggest small peptides as highly potent and promising candidates for their further development into an anti-inflammatory drug. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=small%20peptides" title="small peptides">small peptides</a>, <a href="https://publications.waset.org/abstracts/search?q=cyclooxygenase" title=" cyclooxygenase"> cyclooxygenase</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=substrate" title=" substrate"> substrate</a> </p> <a href="https://publications.waset.org/abstracts/160257/design-synthesis-and-evaluation-of-small-peptides-for-managing-inflammation-inhibition-to-substrate-approach" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/160257.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">88</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">535</span> Links between Inflammation and Insulin Resistance in Children with Morbid Obesity and Metabolic Syndrome</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Mustafa%20M.%20Donma">Mustafa M. Donma</a>, <a href="https://publications.waset.org/abstracts/search?q=Orkide%20Donma"> Orkide Donma</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Obesity is a clinical state associated with low-grade inflammation. It is also a major risk factor for insulin resistance (IR). In its advanced stages, metabolic syndrome (MetS), a much more complicated disease which may lead to life-threatening problems, may develop. Obesity-mediated IR seems to correlate with the inflammation. Human studies performed particularly on pediatric population are scarce. The aim of this study is to detect possible associations between inflammation and IR in terms of some related ratios. 549 children were grouped according to their age- and sex-based body mass index (BMI) percentile tables of WHO. MetS components were determined. Informed consent and approval from the Ethics Committee for Clinical Investigations were obtained. The principles of the Declaration of Helsinki were followed. The exclusion criteria were infection, inflammation, chronic diseases and those under drug treatment. Anthropometric measurements were obtained. Complete blood cell, fasting blood glucose, insulin, and C-reactive protein (CRP) analyses were performed. Homeostasis model assessment of insulin resistance (HOMA-IR), systemic immune inflammation (SII) index, tense index, alanine aminotransferase to aspartate aminotransferase ratio (ALT/AST), neutrophils to lymphocyte (NLR), platelet to lymphocyte, and lymphocyte to monocyte ratios were calculated. Data were evaluated by statistical analyses. The degree for statistical significance was 0.05. Statistically significant differences were found among the BMI values of the groups (p < 0.001). Strong correlations were detected between the BMI and waist circumference (WC) values in all groups. Tense index values were also correlated with both BMI and WC values in all groups except overweight (OW) children. SII index values of children with normal BMI were significantly different from the values obtained in OW, obese, morbid obese and MetS groups. Among all the other lymphocyte ratios, NLR exhibited a similar profile. Both HOMA-IR and ALT/AST values displayed an increasing profile from N towards MetS3 group. BMI and WC values were correlated with HOMA-IR and ALT/AST. Both in morbid obese and MetS groups, significant correlations between CRP versus SII index as well as HOMA-IR versus ALT/AST were found. ALT/AST and HOMA-IR values were correlated with NLR in morbid obese group and with SII index in MetS group, (p < 0.05), respectively. In conclusion, these findings showed that some parameters may exhibit informative differences between the early and late stages of obesity. Important associations among HOMA-IR, ALT/AST, NLR and SII index have come to light in the morbid obese and MetS groups. This study introduced the SII index and NLR as important inflammatory markers for the discrimination of normal and obese children. Interesting links were observed between inflammation and IR in morbid obese children and those with MetS, both being late stages of obesity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=children" title="children">children</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=insulin%20resistance" title=" insulin resistance"> insulin resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=metabolic%20syndrome" title=" metabolic syndrome"> metabolic syndrome</a>, <a href="https://publications.waset.org/abstracts/search?q=obesity" title=" obesity"> obesity</a> </p> <a href="https://publications.waset.org/abstracts/100962/links-between-inflammation-and-insulin-resistance-in-children-with-morbid-obesity-and-metabolic-syndrome" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/100962.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">136</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">534</span> Auricular Electroacupuncture Rescued Epilepsy Seizure by Attenuating TLR-2 Inflammatory Pathway in the Kainic Acid-Induced Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=I-Han%20Hsiao">I-Han Hsiao</a>, <a href="https://publications.waset.org/abstracts/search?q=Chun-Ping%20Huang"> Chun-Ping Huang</a>, <a href="https://publications.waset.org/abstracts/search?q=Ching-Liang%20Hsieh"> Ching-Liang Hsieh</a>, <a href="https://publications.waset.org/abstracts/search?q=Yi-Wen%20Lin"> Yi-Wen Lin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Epilepsy is chronic brain disorder that results in the sporadic occurrence of spontaneous seizures in the temporal lobe, cerebral cortex, and hippocampus. Clinical antiepileptic medicines are often ineffective or little benefits in the small amount of patients and usually initiate severe side effects. This inflammation contributes to enhanced neuronal excitability and the onset of epilepsy. Auricular electric-stimulation (AES) can increase parasympathetic activity and stimulate the solitary tract nucleus to induce the cholinergic anti-inflammatory pathway. Furthermore, it may be a therapeutic strategy for the treatment of epilepsy. In the present study, we want to investigate the effects of AES on inflammatory mediators in kainic acid (KA)-induced epileptic seizure rats. Experimental KA injection increased expression of TLR-2 pathway associated inflammatory mediators, were further reduced by either 2Hz or 15 Hz AES in the prefrontal cortex, hippocampus, and somatosensory cortex. We suggest that AES can successfully control the epileptic seizure by down-regulation of inflammation signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=auricular%20electric-stimulation" title="auricular electric-stimulation">auricular electric-stimulation</a>, <a href="https://publications.waset.org/abstracts/search?q=epileptic%20seizures" title=" epileptic seizures"> epileptic seizures</a>, <a href="https://publications.waset.org/abstracts/search?q=anti-inflammation" title=" anti-inflammation"> anti-inflammation</a> </p> <a href="https://publications.waset.org/abstracts/84898/auricular-electroacupuncture-rescued-epilepsy-seizure-by-attenuating-tlr-2-inflammatory-pathway-in-the-kainic-acid-induced-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/84898.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">185</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">533</span> Role of Sulforaphane on Alleviating Duchenne Muscular Dystrophy(DMD) through Activation of Nrf2</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Sulforaphane (SFN) possesses powerful chemo-preventive effects and plays a crucial role on oxidative stress and inflammatory. In our recent study, SFN treatment could relieve muscular dystrophy in mdx mice by activating Nrf2 (NF-E2 related factor 2). Moreover, our findings indicated that SFN-activated Nrf2 alleviated muscle inflammation in dystrophin-deficient mdx mice through suppressing NF-κB signaling pathway. Collectively, SFN-induced Nrf2 molecular pathway might be a promising approach for treatment of the patients with Duchenne muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Duchenne%20muscular%20dystrophy" title=" Duchenne muscular dystrophy"> Duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/41533/role-of-sulforaphane-on-alleviating-duchenne-muscular-dystrophydmd-through-activation-of-nrf2" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41533.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">214</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">532</span> Regulation on Macrophage and Insulin Resistance after Aerobic Exercise in High-Fat Diet Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Qiaofeng%20Guo">Qiaofeng Guo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aims: Obesity is often accompanied by insulin resistance (IR) and whole-body inflammation. Aerobic exercise is an effective treatment to improve insulin resistance and inflammation. However, the anti-inflammatory mechanisms of exercise on epididymal and subcutaneous adipose remain to be elucidated. Here, we compared the macrophage polarization between epididymal and subcutaneous adipose after aerobic exercise. Methods: Male C57BL/6 mice were fed a normal diet group or a high-fat diet group for 12 weeks and performed aerobic training on a treadmill at 55%~65% VO₂ max for eight weeks. Food intake, body weight, and fasting blood glucose levels were monitored weekly. The intraperitoneal glucose tolerance test was to evaluate the insulin resistance model. Fat mass, blood lipid profile, serum IL-1β, TNF-α levels, and CD31/CD206 rates were analysed after the intervention. Results: FBG (P<0.01), AUCIPGTT (P<0.01), and HOMA-IR (P<0.01) increased significantly for a high-fat diet and decreased significantly after the exercise. Eight weeks of aerobic exercise attenuated HFD-induced weight gain and glucose intolerance and improved insulin sensitivity. Serum IL-1β, TNF-α, CD11C/CD206 expression in subcutaneous adipose tissue were not changed before and after exercise, but not in epididymal adipose tissue (P<0.01). Conclusion: Insulin resistance is not accompanied by chronic inflammation and M1 polarization of subcutaneous adipose tissue macrophages in high-fat diet mice. Aerobic exercise effectively improved lipid metabolism and insulin sensitivity, which may be closely associated with reduced M1 polarization of epididymal adipose macrophages. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=aerobic%20exercise" title="aerobic exercise">aerobic exercise</a>, <a href="https://publications.waset.org/abstracts/search?q=insulin%20resistance" title=" insulin resistance"> insulin resistance</a>, <a href="https://publications.waset.org/abstracts/search?q=chronic%20inflammation" title=" chronic inflammation"> chronic inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=adipose" title=" adipose"> adipose</a>, <a href="https://publications.waset.org/abstracts/search?q=macrophage%20polarization" title=" macrophage polarization"> macrophage polarization</a> </p> <a href="https://publications.waset.org/abstracts/161042/regulation-on-macrophage-and-insulin-resistance-after-aerobic-exercise-in-high-fat-diet-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/161042.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">78</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">531</span> Evaluation of Immunology of Asthma Chronic Obstructive</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Milad%20Gholizadeh">Milad Gholizadeh</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Asthma and chronic obstructive pulmonary disease (COPD) are very shared inflammatory diseases of the airlines. They togethercause airway tapering and are cumulative in occurrence throughout the world, imposing huge burdens on health care. It is currently recognized that some asthmatic inflammation is neutrophilic, controlled by the TH17 subset of helper T cells, and that some eosinophilic inflammation is controlled by type 2 innate lymphoid cells (ILC2 cells) temporary together with basophils. Patients who have plain asthma or are asthmatic patients who smoke with topographies of COPD-induced inflammation and might advantage from treatments targeting neutrophils, countingmacrolides, CXCR2 antagonists, phosphodiesterase 4 inhibitors, p38 mitogen-activating protein kinase inhibitors, and antibodies in contradiction of IL-1 and IL-17.Viral and bacterial infections, not only reason acute exacerbations of COPD, but also intensify and continue chronic inflammation in steady COPD through pathogen-associated molecular patterns. Present treatment plans are absorbed on titration of inhaled therapies such as long-acting bronchodilators, with cumulative interest in the usage of beleaguered biologic therapies meant at the underlying inflammatory devices. Educationssuggest that the mucosal IgA reply is abridged in COPD, and a lacking conveyance of IgA across the bronchial epithelium in COPD has been recognized, perhaps involving neutrophil proteinases, which may damage the Ig receptor mediating this transepithelialdirection-finding. Future instructions for investigation will emphasis elucidating the diverse inflammatory signatures foremost to asthma and chronic obstrucive, the development of reliable analytic standards and biomarkers of illness, and refining the clinical organization with an eye toward targeted therapies. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=imminology" title="imminology">imminology</a>, <a href="https://publications.waset.org/abstracts/search?q=asthma" title=" asthma"> asthma</a>, <a href="https://publications.waset.org/abstracts/search?q=COPD" title=" COPD"> COPD</a>, <a href="https://publications.waset.org/abstracts/search?q=CXCR2%20antagonists" title=" CXCR2 antagonists"> CXCR2 antagonists</a> </p> <a href="https://publications.waset.org/abstracts/143743/evaluation-of-immunology-of-asthma-chronic-obstructive" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/143743.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">162</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">530</span> Caspase-11 and AIM2 Inflammasome are Involved in Smoking-Induced COPD and Lung Adenocarcinoma</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chiara%20Colarusso">Chiara Colarusso</a>, <a href="https://publications.waset.org/abstracts/search?q=Michela%20Terlizzi"> Michela Terlizzi</a>, <a href="https://publications.waset.org/abstracts/search?q=Aldo%20Pinto"> Aldo Pinto</a>, <a href="https://publications.waset.org/abstracts/search?q=Rosalinda%20Sorrentino"> Rosalinda Sorrentino</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Cigarette smoking is the main cause and the most common risk factor for both COPD and lung cancer. In our previous studies, we proved that caspase-11 in mice and its human analogue, caspase-4, are involved in lung carcinogenesis and that AIM2 inflammasome might play a pro-cancerous role in lung cancer. Therefore, the aim of this study was to investigate potential crosstalk between COPD and lung cancer, focusing on AIM2 and caspase-11-dependent inflammasome signaling pathway. To mimic COPD, we took advantage of an experimental first-hand smoking mouse model and, to confirm what was observed in mice, we used human samples of lung adenocarcinoma patients stratified according to the smoking and COPD status. We demonstrated that smoke exposure led to emphysema-like features, bronchial tone impairment, and release of IL-1-like cytokines (IL-1α, IL-1β, IL-33, IL-18) in a caspase-1 independent manner in C57Bl/6N. Rather, a dysfunctional caspase-11 in smoke-exposed 129Sv mice was associated to lower bronchial inflammation, collagen deposition, and IL-1-like inflammation. In addition, for the first time, we found that AIM2 inflammasome is involved in lung inflammation in smoking and COPD, in that its expression was higher in smoke-exposed C57Bl/6N compared to 129Sv smoking mice, who instead did not show any alteration of AIM2 in both macrophages and dendritic cells. Moreover, we found that AIM2 expression in the cancerous tissue, albeit higher than non-cancerous tissue, was not statistically different according to the COPD and smoking status. Instead, the higher expression of AIM2 in non-cancerous tissue of smoker COPD patients than smokers who did not have COPD was correlated to a higher hazard ratio of poor survival rate than patients who presented lower levels of AIM2. In conclusion, our data highlight that caspase-11 in mice is associated to smoke-induced lung latent inflammation which could drive the establishment of lung cancer, and that AIM2 inflammasome plays a role at the crosstalk between smoking/COPD and lung adenocarcinoma in that its higher presence is correlated to lower survival rate of smoker COPD adenocarcinoma. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=COPD" title="COPD">COPD</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammasome" title=" inflammasome"> inflammasome</a>, <a href="https://publications.waset.org/abstracts/search?q=lung%20cancer" title=" lung cancer"> lung cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=lung%20inflammation" title=" lung inflammation"> lung inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=smoke" title=" smoke"> smoke</a> </p> <a href="https://publications.waset.org/abstracts/143446/caspase-11-and-aim2-inflammasome-are-involved-in-smoking-induced-copd-and-lung-adenocarcinoma" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/143446.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">156</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">529</span> Albendazole Ameliorates Inflammatory Response in a Rat Model of Acute Mesenteric Ischemia Reperfusion Injury</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Kamyar%20Moradi">Kamyar Moradi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Acute mesenteric ischemia is known as a life-threatening condition. Re-establishment of blood flow in this condition can lead to mesenteric ischemia reperfusion (MIR) injury, which is accompanied by inflammatory response. Still, clear blueprint of inflammatory mechanism underlying MIR injury has not been provided. Interestingly, Albendazole has exhibited notable effects on inflammation and cytokine production. In this study, we aimed to evaluate outcomes of MIR injury following pretreatment with Albendazole with respect to assessment of mesenteric inflammation and ischemia threshold. Methods: Male rats were randomly divided into sham operated, vehicle treated, Albendazole 100 mg/kg, and Albendazole 200 mg/kg groups. MIR injury was induced by occlusion of superior mesenteric artery for 30 minutes followed by 120 minutes of reperfusion. Samples were utilized for assessment of epithelial survival and villous height. Immunohistochemistry study revealed intestinal expression of TNF-α and HIF-1-α. Gene expression of NF-κB/TLR4/TNF-α/IL-6 was measured using RTPCR. Also, protein levels of inflammatory cytokines in serum and intestine were assessed by ELISA method. Results: Histopathological study demonstrated that pretreatment with Albendazole could ameliorate decline in villous height and epithelial survival following MIR injury. Also, systemic inflammation was suppressed after administration of Albendazole. Analysis of possible participating inflammatory pathway could demonstrate that intestinal expression of NF-κB/TLR4/TNF-α/IL-6 is significantly attenuated in treated groups. Eventually, IHC study illustrated concordant decline in mesenteric expression of HIF-1-α/TNF-α. Conclusion: Single dose pretreatment with Albendazole could ameliorate inflammatory response and enhance ischemia threshold following induction of MIR injury. Still, more studies would clarify existing causality in this phenomenon. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=albendazole" title="albendazole">albendazole</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia%20reperfusion%20injury" title=" ischemia reperfusion injury"> ischemia reperfusion injury</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=mesenteric%20ischemia" title=" mesenteric ischemia"> mesenteric ischemia</a> </p> <a href="https://publications.waset.org/abstracts/146614/albendazole-ameliorates-inflammatory-response-in-a-rat-model-of-acute-mesenteric-ischemia-reperfusion-injury" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/146614.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">169</span> </span> </div> </div> <ul class="pagination"> <li class="page-item disabled"><span class="page-link">&lsaquo;</span></li> <li class="page-item active"><span class="page-link">1</span></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=inflammation&page=2">2</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=inflammation&page=3">3</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=inflammation&page=4">4</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=inflammation&page=5">5</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=inflammation&page=6">6</a></li> <li class="page-item"><a class="page-link" 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