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10.3892/etm.2017.4473 http://scihub22266oqcxt.onion/10.3892/etm.2017.4473 C5488603!5488603!28672952     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Exp+Ther+Med 2017 ; 14 (1): 447-52 Nephropedia Template TP {{tp|p=28672952|t=2017. Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation |pdf=|usr=}}{{28672952}} gab.com Text Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation JO: Exp Ther Med http://www.kidney.de/pget.php?&tw=1&pmid=28672952 #FOAvip The aim of the present study was to determine the effects of emodin, a natural compound with antioxidant properties, on oxidative stress and apoptosis induced by hypoxia/reoxygenation (H/R) in HK-2 human renal tubular cells. In HK-2 cells subjected to H/R, it was observed that pre-treatment with emodin lead to an increase in cellular viability and a reduction in the rate of apoptosis and the B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 ratio. H/R alone caused a significant increase in the levels of reactive oxygen species and malondialdehyde (P<0.05) and a significant decrease in the activities of superoxide dismutase, catalase and glutathione peroxidase (P<0.05), relative to normoxic cells. In turn, parameters of oxidative stress were improved by emodin pre-treatment. In addition, emodin pre-treatment significantly inhibited the phosphorylation of extracellular signal-regulated protein kinase and c-Jun N-terminal kinase mitogen-activated protein kinases (MAPKs) induced by H/R (P<0.05). These data suggest that emodin may prevent H/R-induced apoptosis in human renal tubular cells through the regulation of cellular oxidative stress, MAPK activation and restoration of the Bax/Bcl-2 ratio. Twit Text FOAVip Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation ????Exp Ther Med http://www.kidney.de/pget.php?&tw=1&pmid=28672952 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28672952 #FOAvip English Wikipedia <ref>{{Cite pmid|28672952}}</ref> Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation #MMPMID28672952 Chen H; Huang RS; Yu XX; Ye Q; Pan LL; Shao GJ; Pan J Exp Ther Med 2017[Jul]; 14 (1): 447-52 PMID28672952show ga The aim of the present study was to determine the effects of emodin, a natural compound with antioxidant properties, on oxidative stress and apoptosis induced by hypoxia/reoxygenation (H/R) in HK-2 human renal tubular cells. In HK-2 cells subjected to H/R, it was observed that pre-treatment with emodin lead to an increase in cellular viability and a reduction in the rate of apoptosis and the B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 ratio. H/R alone caused a significant increase in the levels of reactive oxygen species and malondialdehyde (P<0.05) and a significant decrease in the activities of superoxide dismutase, catalase and glutathione peroxidase (P<0.05), relative to normoxic cells. In turn, parameters of oxidative stress were improved by emodin pre-treatment. In addition, emodin pre-treatment significantly inhibited the phosphorylation of extracellular signal-regulated protein kinase and c-Jun N-terminal kinase mitogen-activated protein kinases (MAPKs) induced by H/R (P<0.05). These data suggest that emodin may prevent H/R-induced apoptosis in human renal tubular cells through the regulation of cellular oxidative stress, MAPK activation and restoration of the Bax/Bcl-2 ratio. äEmodin protects against oxidative stress and apoptosis in HK-2 renal t(epmc).pdf DeepDyve Pubget Overpricing