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10.1016/j.ebiom.2017.03.021 http://scihub22266oqcxt.onion/10.1016/j.ebiom.2017.03.021 C5405163!5405163!28330809     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EBioMedicine 2017 ; 18 (ä): 179-87 Nephropedia Template TP {{tp|p=28330809|t=2017. Piperine Attenuates Pathological Cardiac Fibrosis Via PPAR-?/AKT Pathways |pdf=|usr=}}{{28330809}} gab.com Text Piperine Attenuates Pathological Cardiac Fibrosis Via PPAR- /AKT Pathways JO: EBioMedicine http://www.kidney.de/pget.php?&tw=1&pmid=28330809 #FOAvip Mitogen-activated protein kinases (MAPKs) and AMP­activated protein kinase ? (AMPK?) play critical roles in the process of cardiac hypertrophy. Previous studies have demonstrated that piperine activates AMPK? and reduces the phosphorylation of extracellular signal-regulated kinase (ERK). However, the effect of piperine on cardiac hypertrophy remains completely unknown. Here, we show that piperine-treated mice had similar hypertrophic responses as mice treated with vehicle but exhibited significantly attenuated cardiac fibrosis after pressure overload or isoprenaline (ISO) injection. Piperine inhibited the transformation of cardiac fibroblasts to myofibroblasts induced by transforming growth factor-? (TGF-?) or angiotensin II (Ang II) in vitro. This anti-fibrotic effect was independent of the AMPK? and MAPK pathway. Piperine blocked activation of protein kinase B (AKT) and, downstream, glycogen synthase kinase 3? (GSK3?). The overexpression of constitutively active AKT or the knockdown of GSK3? completely abolished the piperine-mediated protection of cardiac fibroblasts. The cardioprotective effects of piperine were blocked in mice with constitutively active AKT. Pretreatment with GW9662, a specific inhibitor of peroxisome proliferator activated receptor-? (PPAR-?), reversed the effect elicited by piperine in vitro. In conclusion, piperine attenuated cardiac fibrosis via the activation of PPAR-? and the resultant inhibition of AKT/GSK3?. Twit Text FOAVip Piperine Attenuates Pathological Cardiac Fibrosis Via PPAR- /AKT Pathways ????EBioMedicine http://www.kidney.de/pget.php?&tw=1&pmid=28330809 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28330809 #FOAvip English Wikipedia <ref>{{Cite pmid|28330809}}</ref> Piperine Attenuates Pathological Cardiac Fibrosis Via PPAR-?/AKT Pathways #MMPMID28330809 Ma ZG; Yuan YP; Zhang X; Xu SC; Wang SS; Tang QZ EBioMedicine 2017[Apr]; 18 (ä): 179-87 PMID28330809show ga Mitogen-activated protein kinases (MAPKs) and AMP­activated protein kinase ? (AMPK?) play critical roles in the process of cardiac hypertrophy. Previous studies have demonstrated that piperine activates AMPK? and reduces the phosphorylation of extracellular signal-regulated kinase (ERK). However, the effect of piperine on cardiac hypertrophy remains completely unknown. Here, we show that piperine-treated mice had similar hypertrophic responses as mice treated with vehicle but exhibited significantly attenuated cardiac fibrosis after pressure overload or isoprenaline (ISO) injection. Piperine inhibited the transformation of cardiac fibroblasts to myofibroblasts induced by transforming growth factor-? (TGF-?) or angiotensin II (Ang II) in vitro. This anti-fibrotic effect was independent of the AMPK? and MAPK pathway. Piperine blocked activation of protein kinase B (AKT) and, downstream, glycogen synthase kinase 3? (GSK3?). The overexpression of constitutively active AKT or the knockdown of GSK3? completely abolished the piperine-mediated protection of cardiac fibroblasts. The cardioprotective effects of piperine were blocked in mice with constitutively active AKT. Pretreatment with GW9662, a specific inhibitor of peroxisome proliferator activated receptor-? (PPAR-?), reversed the effect elicited by piperine in vitro. In conclusion, piperine attenuated cardiac fibrosis via the activation of PPAR-? and the resultant inhibition of AKT/GSK3?. äPiperine Attenuates Pathological Cardiac Fibrosis Via PPAR-?/AKT Pathw(epmc).pdf DeepDyve Pubget Overpricing