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10.1111/hepr.12352 http://scihub22266oqcxt.onion/10.1111/hepr.12352 C4219935!4219935!24796378     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hepatol+Res 2015 ; 45 (3): 305-14 Nephropedia Template TP {{tp|p=24796378|t=2015. Inhibition of Acidic Sphingomyelinase Reduces Established Hepatic Fibrosis in Mice |pdf=|usr=}}{{24796378}} gab.com Text Inhibition of Acidic Sphingomyelinase Reduces Established Hepatic Fibrosis in Mice JO: Hepatol Res http://www.kidney.de/pget.php?&tw=1&pmid=24796378 #FOAvip Aims: Liver fibrosis occurs as a result of several chronic liver diseases and leads to portal hypertension, cirrhosis and liver failure, often requiring liver transplantation. Activated hepatic stellate cells (HSC) are known to contribute to liver fibrosis, but currently there are no effective therapies for the treatment of established liver fibrosis. Activation of the acidic sphingomyelinase (ASM) has been shown to be involved in HSC activation. In the present study we investigated whether treatment with the ASM inhibitor, amitriptyline (TCA), could prevent and/or reverse fibrosis induced in mice by carbon tetrachloride (CCl4). Methods: Mice were treated with CCl4 for 8 weeks to induce fibrosis. Concurrently, mice received drinking water with or without 180 mg/L TCA. Results: Mice receiving TCA in the water had decreased hepatic collagen deposition and reduced liver mRNA expression of the fibrogenic mediators, TGF-?1, TIMP-1, collagen, and TNF?. TCA treatment also reduced HSC activation determined by ?-smooth muscle actin staining. In a separate set of experiments, mice were treated with CCl4 for 5 weeks prior to treatment with TCA, to test whether TCA had any effect on established fibrosis. Remarkably, in mice with established fibrosis, treatment with TCA significantly reduced collagen deposition, HSC activation, and prevented portal hypertension and improved hepatic architecture. Treatment of isolated HSC in vitro with TCA completely inhibited TGF-?1-induced collagen expression and PDGF-BB-induced proliferation. Conclusions: The data suggest that ASM is a critical signaling component in HSC for the development of liver fibrosis and represents an important therapeutic target. Twit Text FOAVip Inhibition of Acidic Sphingomyelinase Reduces Established Hepatic Fibrosis in Mice ????Hepatol Res http://www.kidney.de/pget.php?&tw=1&pmid=24796378 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24796378 #FOAvip English Wikipedia <ref>{{Cite pmid|24796378}}</ref> Inhibition of Acidic Sphingomyelinase Reduces Established Hepatic Fibrosis in Mice #MMPMID24796378 Quillin RC; Wilson GC; Nojima H; Freeman CH; Wang J; Schuster RM; Blanchard JA; Edwards MJ; Gandhi CR; Gulbins E; Lentsch AB Hepatol Res 2015[Mar]; 45 (3): 305-14 PMID24796378show ga Aims: Liver fibrosis occurs as a result of several chronic liver diseases and leads to portal hypertension, cirrhosis and liver failure, often requiring liver transplantation. Activated hepatic stellate cells (HSC) are known to contribute to liver fibrosis, but currently there are no effective therapies for the treatment of established liver fibrosis. Activation of the acidic sphingomyelinase (ASM) has been shown to be involved in HSC activation. In the present study we investigated whether treatment with the ASM inhibitor, amitriptyline (TCA), could prevent and/or reverse fibrosis induced in mice by carbon tetrachloride (CCl4). Methods: Mice were treated with CCl4 for 8 weeks to induce fibrosis. Concurrently, mice received drinking water with or without 180 mg/L TCA. Results: Mice receiving TCA in the water had decreased hepatic collagen deposition and reduced liver mRNA expression of the fibrogenic mediators, TGF-?1, TIMP-1, collagen, and TNF?. TCA treatment also reduced HSC activation determined by ?-smooth muscle actin staining. In a separate set of experiments, mice were treated with CCl4 for 5 weeks prior to treatment with TCA, to test whether TCA had any effect on established fibrosis. Remarkably, in mice with established fibrosis, treatment with TCA significantly reduced collagen deposition, HSC activation, and prevented portal hypertension and improved hepatic architecture. Treatment of isolated HSC in vitro with TCA completely inhibited TGF-?1-induced collagen expression and PDGF-BB-induced proliferation. Conclusions: The data suggest that ASM is a critical signaling component in HSC for the development of liver fibrosis and represents an important therapeutic target. äInhibition of Acidic Sphingomyelinase Reduces Established Hepatic Fibr(epmc).pdf DeepDyve Pubget Overpricing