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http://scihub22266oqcxt.onion/ C4152036!4152036!25197346     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Int+J+Clin+Exp+Pathol 2014 ; 7 (8): 4755-64 Nephropedia Template TP {{tp|p=25197346|t=2014. Magnesium isoglycyrrhizinate protects hepatic L02 cells from ischemia/reperfusion induced injury |pdf=|usr=}}{{25197346}} gab.com Text Magnesium isoglycyrrhizinate protects hepatic L02 cells from ischemia/reperfusion induced injury JO: Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=25197346 #FOAvip Human liver ischemia/reperfusion injury (IRI) is a common and major clinical problem complicating liver surgery and transplantation. The pathogenesis underlying IRI is complex, involving a series of signaling mediators and mechanisms. This study aimed to investigate the effects of Magnesium Isoglycyrrhizinate (MgIG) on the changes of oxidant stress and apoptosis induced by IRI in human hepatic L02 cells. L02 cells with IRI were treated with or without MgIG and mitoKATP (Mitochondrial adenosine triphosphate-dependent potassium) channel modulators. Cell viability was assessed using CCK-8 assay. Cell apoptosis was quantified by flow cytometry. The activity of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured. Effects of MgIG on the expression of Bax, Bcl-2, Caspase 3, PARP (poly ADP-ribose polymerase), Akt, and ERK in L02 cells with IRI were examined. Our results showed that MgIG treatment significantly reduced the population of apoptotic cells and the expression of apoptosis-related proteins in hepatic L02 cells with IRI. MgIG also counteract ischemia reperfusion induced oxidative challenge as it effectively reduced malondialdehyde (MDA) and increased the activities of SOD and GSH-Px. L02 cells treated with MgIG showed increased expression of p-Akt and p-ERK, indicating that the protective effect of MgIG might be associated with the activation of Akt and ERK pathways. Moreover, the addition of Diazoxide (DE), a mitoKATP channel opener, enhanced the cytoprotective activity of MgIG, while the mitoKATP blocker 5-hydroxydecanoate (5-HD) reduced the cytoprotective activity of MgIG. Twit Text FOAVip Magnesium isoglycyrrhizinate protects hepatic L02 cells from ischemia/reperfusion induced injury ????Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=25197346 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25197346 #FOAvip English Wikipedia <ref>{{Cite pmid|25197346}}</ref> Magnesium isoglycyrrhizinate protects hepatic L02 cells from ischemia/reperfusion induced injury #MMPMID25197346 Huang X; Qin J; Lu S Int J Clin Exp Pathol 2014[]; 7 (8): 4755-64 PMID25197346show ga Human liver ischemia/reperfusion injury (IRI) is a common and major clinical problem complicating liver surgery and transplantation. The pathogenesis underlying IRI is complex, involving a series of signaling mediators and mechanisms. This study aimed to investigate the effects of Magnesium Isoglycyrrhizinate (MgIG) on the changes of oxidant stress and apoptosis induced by IRI in human hepatic L02 cells. L02 cells with IRI were treated with or without MgIG and mitoKATP (Mitochondrial adenosine triphosphate-dependent potassium) channel modulators. Cell viability was assessed using CCK-8 assay. Cell apoptosis was quantified by flow cytometry. The activity of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured. Effects of MgIG on the expression of Bax, Bcl-2, Caspase 3, PARP (poly ADP-ribose polymerase), Akt, and ERK in L02 cells with IRI were examined. Our results showed that MgIG treatment significantly reduced the population of apoptotic cells and the expression of apoptosis-related proteins in hepatic L02 cells with IRI. MgIG also counteract ischemia reperfusion induced oxidative challenge as it effectively reduced malondialdehyde (MDA) and increased the activities of SOD and GSH-Px. L02 cells treated with MgIG showed increased expression of p-Akt and p-ERK, indicating that the protective effect of MgIG might be associated with the activation of Akt and ERK pathways. Moreover, the addition of Diazoxide (DE), a mitoKATP channel opener, enhanced the cytoprotective activity of MgIG, while the mitoKATP blocker 5-hydroxydecanoate (5-HD) reduced the cytoprotective activity of MgIG. äMagnesium isoglycyrrhizinate protects hepatic L02 cells from ischemia/(epmc).pdf DeepDyve Pubget Overpricing