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http://scihub22266oqcxt.onion/ C4767450!4767450!26729705     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2015 ; 6 (40): 42530-40 Nephropedia Template TP {{tp|p=26729705|t=2015. Oleoylethanolamide, an endogenous PPAR-? ligand, attenuates liver fibrosis targeting hepatic stellate cells |pdf=|usr=}}{{26729705}} gab.com Text Oleoylethanolamide, an endogenous PPAR- ligand, attenuates liver fibrosis targeting hepatic stellate cells JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26729705 #FOAvip Oleoylethanolamide (OEA), an endocannabinoid-like molecule, was revealed to modulate lipid metabolism through a peroxisome proliferator-activated receptor-? (PPAR-?) mediated mechanism. In present study, we further investigated the activities and mechanisms of OEA in ameliorating hepatic fibrosis in Sv/129 mice induced by a methionine choline-deficient (MCD) diet or thioacetamide (TAA) treatment. Liver fibrosis development was assessed by Hematoxylin-eosin and Sirius red staining. Treatment with OEA (5 mg/kg/day, intraperitoneal injection, i.p.) significantly attenuated the progress of liver fibrosis in both two experimental animal models by blocking the activation of hepatic stellate cells (HSCs). Gene expression analysis of hepatic tissues indicated that OEA inhibited the expression of ?-smooth muscle action (?-SMA) and collagen matrix, fibrosis markers, and genes involved in inflammation and extracellular matrix remodeling. In vitro studies showed that OEA inhibited transforming growth factor ?1-stimulated HSCs activation through suppressing Smad2/3 phosphorylation, ?-SMA expression and myofibroblast transformation. These improvements could not be observed in PPAR-? knockout mice models with OEA administration, which suggested all the anti-fibrotic effects of OEA in vivo and in vitro were mediated by PPAR-? activation. Collectively, our results suggested that OEA exerted a pharmacological effect on modulating hepatic fibrosis development through the inhibition of HSCs activation in liver and therefore may be a potential therapeutic agent for liver fibrosis. Twit Text FOAVip Oleoylethanolamide, an endogenous PPAR- ligand, attenuates liver fibrosis targeting hepatic stellate cells ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26729705 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26729705 #FOAvip English Wikipedia <ref>{{Cite pmid|26729705}}</ref> Oleoylethanolamide, an endogenous PPAR-? ligand, attenuates liver fibrosis targeting hepatic stellate cells #MMPMID26729705 Chen L; Li L; Chen J; Li L; Zheng Z; Ren J; Qiu Y Oncotarget 2015[Dec]; 6 (40): 42530-40 PMID26729705show ga Oleoylethanolamide (OEA), an endocannabinoid-like molecule, was revealed to modulate lipid metabolism through a peroxisome proliferator-activated receptor-? (PPAR-?) mediated mechanism. In present study, we further investigated the activities and mechanisms of OEA in ameliorating hepatic fibrosis in Sv/129 mice induced by a methionine choline-deficient (MCD) diet or thioacetamide (TAA) treatment. Liver fibrosis development was assessed by Hematoxylin-eosin and Sirius red staining. Treatment with OEA (5 mg/kg/day, intraperitoneal injection, i.p.) significantly attenuated the progress of liver fibrosis in both two experimental animal models by blocking the activation of hepatic stellate cells (HSCs). Gene expression analysis of hepatic tissues indicated that OEA inhibited the expression of ?-smooth muscle action (?-SMA) and collagen matrix, fibrosis markers, and genes involved in inflammation and extracellular matrix remodeling. In vitro studies showed that OEA inhibited transforming growth factor ?1-stimulated HSCs activation through suppressing Smad2/3 phosphorylation, ?-SMA expression and myofibroblast transformation. These improvements could not be observed in PPAR-? knockout mice models with OEA administration, which suggested all the anti-fibrotic effects of OEA in vivo and in vitro were mediated by PPAR-? activation. Collectively, our results suggested that OEA exerted a pharmacological effect on modulating hepatic fibrosis development through the inhibition of HSCs activation in liver and therefore may be a potential therapeutic agent for liver fibrosis. äOleoylethanolamide, an endogenous PPAR-? ligand, attenuates liver fibr(epmc).pdf DeepDyve Pubget Overpricing