Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

http://scihub22266oqcxt.onion/ C4503123!4503123!26191252     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Clin+Exp+Pathol 2015 ; 8 (5): 5471-7 Nephropedia Template TP {{tp|p=26191252|t=2015. Inhibitory effects of dimethyl ?-ketoglutarate in hepatic stellate cell activation |pdf=|usr=}}{{26191252}} gab.com Text Inhibitory effects of dimethyl -ketoglutarate in hepatic stellate cell activation JO: Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26191252 #FOAvip Aim: The activation of Hepatic stellate cell (HSC) is a pivotal event in the initiation and progression of hepatic fibrosis and a major source of collagen deposition. A recent study found that autophagy fuels the HSC activation. ?-ketoglutarate (AKG), an intermediate in the Kerbs CYCLE, has been shown to regulate the level of autophagy. In this study, we aim to investigate the potential effect of dimethyl ?-ketoglutarate (DMKG), a membrane-permeable esters of AKG, on the activation of HSC. Methods: HSC and hepatocyte cell lines were treated with DMKG at gradient concentrations, MTT assay was used to assess the cell viability. Concentrations of DMKG that did not affect the cell survival were added to the culture media of HSC cells. Real-time PCR and western blot analysis was carried out to evaluate the expression of fibrogenic genes in HSC after culture for 24 hours. Results: Low dose of DMKG had little cytotoxicity to both HSCs and hepatocytes, while HSCs were more vulnerable to high dose of DMKG than hepatocytes. More importantly, DMKG inhibited the expression of ?-SMA and collagen I significantly in HSCs detected by real-time PCR and western blot analysis at the concentrations that didn?t decrease cell viability. Conclusions: DMKG has a significant role of inhibiting the activation of HSC and may attenuate hepatic fibrosis safely. Twit Text FOAVip Inhibitory effects of dimethyl -ketoglutarate in hepatic stellate cell activation ????Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26191252 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26191252 #FOAvip English Wikipedia <ref>{{Cite pmid|26191252}}</ref> Inhibitory effects of dimethyl ?-ketoglutarate in hepatic stellate cell activation #MMPMID26191252 Zhao J; Peng L; Luo Z; Cui R; Yan M Int J Clin Exp Pathol 2015[]; 8 (5): 5471-7 PMID26191252show ga Aim: The activation of Hepatic stellate cell (HSC) is a pivotal event in the initiation and progression of hepatic fibrosis and a major source of collagen deposition. A recent study found that autophagy fuels the HSC activation. ?-ketoglutarate (AKG), an intermediate in the Kerbs CYCLE, has been shown to regulate the level of autophagy. In this study, we aim to investigate the potential effect of dimethyl ?-ketoglutarate (DMKG), a membrane-permeable esters of AKG, on the activation of HSC. Methods: HSC and hepatocyte cell lines were treated with DMKG at gradient concentrations, MTT assay was used to assess the cell viability. Concentrations of DMKG that did not affect the cell survival were added to the culture media of HSC cells. Real-time PCR and western blot analysis was carried out to evaluate the expression of fibrogenic genes in HSC after culture for 24 hours. Results: Low dose of DMKG had little cytotoxicity to both HSCs and hepatocytes, while HSCs were more vulnerable to high dose of DMKG than hepatocytes. More importantly, DMKG inhibited the expression of ?-SMA and collagen I significantly in HSCs detected by real-time PCR and western blot analysis at the concentrations that didn?t decrease cell viability. Conclusions: DMKG has a significant role of inhibiting the activation of HSC and may attenuate hepatic fibrosis safely. äInhibitory effects of dimethyl ?-ketoglutarate in hepatic stellate cel(epmc).pdf DeepDyve Pubget Overpricing