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10.1371/journal.pone.0135858 http://scihub22266oqcxt.onion/10.1371/journal.pone.0135858 C4567351!4567351 !26360050     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26360050 &cmd=llinks): Failed to open stream: HTTP request failed! 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Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the STAT3 Signaling Pathway and Regulation of the between Th17/Treg Balance |pdf=|usr=}}{{26360050 }} gab.com Text Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the STAT3 Signaling Pathway and Regulation of the between Th17/Treg Balance JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26360050 #FOAvip OBJECTIVE: Metformin is used to treat type 2 diabetes. We sought to determine whether metformin reduces inflammation, by regulating p-signal transducer and activator of transcription 3 (STAT3) expression and T-helper 17 (Th17) cell proliferation, in a mouse model of inflammatory bowel disease (IBD). METHODS: IBD mice were administered metformin for 16 days and their tissues were analyzed. AMP-activated protein kinase (AMPK), the mammalian target of rapamycin (mTOR), p-STAT3 and p-STAT5 in the spleen and lymph nodes were detected using immunohistochemistry and confocal microscopy. Gene expression was determined using quantitative PCR assays, and protein expression levels were measured using western blotting and enzyme-linked immunosorbent assays. Human HT-29 cell proliferation was evaluated using MTT assays. RESULTS: Metformin reduced disease activity index scores and inhibited weight loss. Metformin also decreased the colonic histological score and inflammatory mediators and increased colon lengths increased. Treatment with metformin inhibited the expression of interleukin (IL)-17, p-STAT3, and p-mTOR. In contrast, metformin treatment increased expression levels of p-AMPK and Foxp3. In addition, expression of inflammatory cytokines decreased in a dose-dependent manner in inflamed human HT-29 cells cultured with metformin at various concentrations. CONCLUSIONS: Metformin attenuates IBD severity and reduces inflammation through the inhibition of p-STAT3 and IL-17 expression. Our results have increased our understanding of this chronic inflammatory disease, and support the strategy of using p-STAT3 inhibitors to treat IBD. Twit Text FOAVip Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the STAT3 Signaling Pathway and Regulation of the between Th17/Treg Balance ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26360050 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26360050 #FOAvip English Wikipedia <ref>{{Cite pmid|26360050 }}</ref> Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the STAT3 Signaling Pathway and Regulation of the between Th17/Treg Balance #MMPMID26360050 Lee SY ; Lee SH ; Yang EJ ; Kim EK ; Kim JK ; Shin DY ; Cho ML PLoS One 2015[]; 10 (9 ): e0135858 PMID26360050 show ga OBJECTIVE: Metformin is used to treat type 2 diabetes. We sought to determine whether metformin reduces inflammation, by regulating p-signal transducer and activator of transcription 3 (STAT3) expression and T-helper 17 (Th17) cell proliferation, in a mouse model of inflammatory bowel disease (IBD). METHODS: IBD mice were administered metformin for 16 days and their tissues were analyzed. AMP-activated protein kinase (AMPK), the mammalian target of rapamycin (mTOR), p-STAT3 and p-STAT5 in the spleen and lymph nodes were detected using immunohistochemistry and confocal microscopy. Gene expression was determined using quantitative PCR assays, and protein expression levels were measured using western blotting and enzyme-linked immunosorbent assays. Human HT-29 cell proliferation was evaluated using MTT assays. RESULTS: Metformin reduced disease activity index scores and inhibited weight loss. Metformin also decreased the colonic histological score and inflammatory mediators and increased colon lengths increased. Treatment with metformin inhibited the expression of interleukin (IL)-17, p-STAT3, and p-mTOR. In contrast, metformin treatment increased expression levels of p-AMPK and Foxp3. In addition, expression of inflammatory cytokines decreased in a dose-dependent manner in inflamed human HT-29 cells cultured with metformin at various concentrations. CONCLUSIONS: Metformin attenuates IBD severity and reduces inflammation through the inhibition of p-STAT3 and IL-17 expression. Our results have increased our understanding of this chronic inflammatory disease, and support the strategy of using p-STAT3 inhibitors to treat IBD. |Animals [MESH] |Cell Differentiation/drug effects/immunology [MESH] |Cell Line [MESH] |Cytokines/genetics/metabolism [MESH] |Disease Models, Animal [MESH] |Gene Expression [MESH] |Humans [MESH] |Inflammation Mediators/metabolism [MESH] |Inflammatory Bowel Diseases/*immunology/*metabolism [MESH] |Metformin/*pharmacology [MESH] |Mice [MESH] |Phosphorylation [MESH] |RNA, Messenger/genetics [MESH] |STAT3 Transcription Factor/*metabolism [MESH] |Signal Transduction/*drug effects [MESH] |T-Lymphocytes, Regulatory/cytology/drug effects/immunology/*metabolism [MESH] |TOR Serine-Threonine Kinases/metabolism [MESH]Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the(epmc).pdf DeepDyve Pubget Overpricing