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10.1371/journal.pone.0120713 http://scihub22266oqcxt.onion/10.1371/journal.pone.0120713 C4376672!4376672!25816210     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 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 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       PLoS+One 2015 ; 10 (3): ä Nephropedia Template TP {{tp|p=25816210|t=2015. Gallic Acid Induces Necroptosis via TNF?? Signaling Pathway in Activated Hepatic Stellate Cells |pdf=|usr=}}{{25816210}} gab.com Text Gallic Acid Induces Necroptosis via TNF Signaling Pathway in Activated Hepatic Stellate Cells JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25816210 #FOAvip Gallic acid (3, 4, 5-trihydroxybenzoic acid, GA), a natural phenolic acid widely found in gallnuts, tea leaves and various fruits, possesses several bioactivities against inflammation, oxidation, and carcinogenicity. The beneficial effect of GA on the reduction of animal hepatofibrosis has been indicated due to its antioxidative property. However, the cytotoxicity of GA autoxidation causing cell death has also been reported. Herein, we postulated that GA might target activated hepatic stellate cells (aHSCs), the cell type responsible for hepatofibrosis, to mitigate the process of fibrosis. The molecular cytotoxic mechanisms that GA exerted on aHSCs were then analyzed. The results indicated that GA elicited aHSC programmed cell death through TNF???mediated necroptosis. GA induced significant oxidative stress through the suppression of catalase activity and the depletion of glutathione (GSH). Elevated oxidative stress triggered the production of TNF?? facilitating the undergoing of necroptosis through the up-regulation of key necroptotic regulatory proteins TRADD and receptor-interacting protein 3 (RIP3), and the inactivation of caspase?8. Calmodulin and calpain?1 activation were engaged, which promoted subsequent lysosomal membrane permeabilization (LMP). The TNF?? antagonist (SPD?304) and the RIP1 inhibitor (necrostatin?1, Nec?1) confirmed GA-induced TNFR1?mediated necroptosis. The inhibition of RIP1 by Nec?1 diverted the cell death from necroptosis to apoptosis, as the activation of caspase 3 and the increase of cytochrome c. Collectively, this is the first report indicating that GA induces TNF signaling?triggered necroptosis in aHSCs, which may offer an alternative strategy for the amelioration of liver fibrosis. Twit Text FOAVip Gallic Acid Induces Necroptosis via TNF Signaling Pathway in Activated Hepatic Stellate Cells ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25816210 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25816210 #FOAvip English Wikipedia <ref>{{Cite pmid|25816210}}</ref> Gallic Acid Induces Necroptosis via TNF?? Signaling Pathway in Activated Hepatic Stellate Cells #MMPMID25816210 Chang YJ; Hsu SL; Liu YT; Lin YH; Lin MH; Huang SJ; Ho Jan A; Wu LC PLoS One 2015[]; 10 (3): ä PMID25816210show ga Gallic acid (3, 4, 5-trihydroxybenzoic acid, GA), a natural phenolic acid widely found in gallnuts, tea leaves and various fruits, possesses several bioactivities against inflammation, oxidation, and carcinogenicity. The beneficial effect of GA on the reduction of animal hepatofibrosis has been indicated due to its antioxidative property. However, the cytotoxicity of GA autoxidation causing cell death has also been reported. Herein, we postulated that GA might target activated hepatic stellate cells (aHSCs), the cell type responsible for hepatofibrosis, to mitigate the process of fibrosis. The molecular cytotoxic mechanisms that GA exerted on aHSCs were then analyzed. The results indicated that GA elicited aHSC programmed cell death through TNF???mediated necroptosis. GA induced significant oxidative stress through the suppression of catalase activity and the depletion of glutathione (GSH). Elevated oxidative stress triggered the production of TNF?? facilitating the undergoing of necroptosis through the up-regulation of key necroptotic regulatory proteins TRADD and receptor-interacting protein 3 (RIP3), and the inactivation of caspase?8. Calmodulin and calpain?1 activation were engaged, which promoted subsequent lysosomal membrane permeabilization (LMP). The TNF?? antagonist (SPD?304) and the RIP1 inhibitor (necrostatin?1, Nec?1) confirmed GA-induced TNFR1?mediated necroptosis. The inhibition of RIP1 by Nec?1 diverted the cell death from necroptosis to apoptosis, as the activation of caspase 3 and the increase of cytochrome c. Collectively, this is the first report indicating that GA induces TNF signaling?triggered necroptosis in aHSCs, which may offer an alternative strategy for the amelioration of liver fibrosis. äGallic Acid Induces Necroptosis via TNF?? Signaling Pathway in Activat(epmc).pdf DeepDyve Pubget Overpricing