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/ C4859875!4859875!27186319     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Physiol+Pathophysiol+Pharmacol 2016 ; 8 (1): 14-27 Nephropedia Template TP {{tp|p=27186319|t=2016. The mitochondria-targeted antioxidant MitoQ attenuates liver fibrosis in mice |pdf=|usr=}}{{27186319}} gab.com Text The mitochondria-targeted antioxidant MitoQ attenuates liver fibrosis in mice JO: Int J Physiol Pathophysiol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=27186319 #FOAvip Oxidative stress plays an essential role in liver fibrosis. This study investigated whether MitoQ, an orally active mitochondrial antioxidant, decreases liver fibrosis. Mice were injected with corn oil or carbon tetrachloride (CCl4, 1:3 dilution in corn oil; 1 µl/g, ip) once every 3 days for up to 6 weeks. 4-Hydroxynonenal adducts increased markedly after CCl4 treatment, indicating oxidative stress. MitoQ attenuated oxidative stress after CCl4. Collagen 1?1 mRNA and hydroxyproline increased markedly after CCl4 treatment, indicating increased collagen formation and deposition. CCl4 caused overt pericentral fibrosis as revealed by both the sirius red staining and second harmonic generation microscopy. MitoQ blunted fibrosis after CCl4. Profibrotic transforming growth factor-?1 (TGF-?1) mRNA and expression of smooth muscle ?-actin, an indicator of hepatic stellate cell (HSC) activation, increased markedly after CCl4 treatment. Smad 2/3, the major mediator of TGF-? fibrogenic effects, was also activated after CCl4 treatment. MitoQ blunted HSC activation, TGF-? expression, and Smad2/3 activation after CCl4 treatment. MitoQ also decreased necrosis, apoptosis and inflammation after CCl4 treatment. In cultured HSCs, MitoQ decreased oxidative stress, inhibited HSC activation, TGF-?1 expression, Smad2/3 activation, and extracellular signal-regulated protein kinase activation. Taken together, these data indicate that mitochondrial reactive oxygen species play an important role in liver fibrosis and that mitochondria-targeted antioxidants are promising potential therapies for prevention and treatment of liver fibrosis. Twit Text FOAVip The mitochondria-targeted antioxidant MitoQ attenuates liver fibrosis in mice ????Int J Physiol Pathophysiol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=27186319 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27186319 #FOAvip English Wikipedia <ref>{{Cite pmid|27186319}}</ref> The mitochondria-targeted antioxidant MitoQ attenuates liver fibrosis in mice #MMPMID27186319 Rehman H; Liu Q; Krishnasamy Y; Shi Z; Ramshesh VK; Haque K; Schnellmann RG; Murphy MP; Lemasters JJ; Rockey DC; Zhong Z Int J Physiol Pathophysiol Pharmacol 2016[]; 8 (1): 14-27 PMID27186319show ga Oxidative stress plays an essential role in liver fibrosis. This study investigated whether MitoQ, an orally active mitochondrial antioxidant, decreases liver fibrosis. Mice were injected with corn oil or carbon tetrachloride (CCl4, 1:3 dilution in corn oil; 1 µl/g, ip) once every 3 days for up to 6 weeks. 4-Hydroxynonenal adducts increased markedly after CCl4 treatment, indicating oxidative stress. MitoQ attenuated oxidative stress after CCl4. Collagen 1?1 mRNA and hydroxyproline increased markedly after CCl4 treatment, indicating increased collagen formation and deposition. CCl4 caused overt pericentral fibrosis as revealed by both the sirius red staining and second harmonic generation microscopy. MitoQ blunted fibrosis after CCl4. Profibrotic transforming growth factor-?1 (TGF-?1) mRNA and expression of smooth muscle ?-actin, an indicator of hepatic stellate cell (HSC) activation, increased markedly after CCl4 treatment. Smad 2/3, the major mediator of TGF-? fibrogenic effects, was also activated after CCl4 treatment. MitoQ blunted HSC activation, TGF-? expression, and Smad2/3 activation after CCl4 treatment. MitoQ also decreased necrosis, apoptosis and inflammation after CCl4 treatment. In cultured HSCs, MitoQ decreased oxidative stress, inhibited HSC activation, TGF-?1 expression, Smad2/3 activation, and extracellular signal-regulated protein kinase activation. Taken together, these data indicate that mitochondrial reactive oxygen species play an important role in liver fibrosis and that mitochondria-targeted antioxidants are promising potential therapies for prevention and treatment of liver fibrosis. äThe mitochondria-targeted antioxidant MitoQ attenuates liver fibrosis (epmc).pdf DeepDyve Pubget Overpricing