Ferric citrate CYP2E1-independently promotes alcohol-induced apoptosis in HepG2 cells via oxidative/nitrative stress which is attenuated by pretreatment with baicalin.
作者： Yan Xu , Yunchao Feng , Hailing Li , Zhonghong Gao
DOI: 10.1016/J.FCT.2012.05.061
关键词:
摘要: In the case of alcoholic liver injury, an iron overload is always present. Both alcohol and can individually induce oxidative stress in liver. However, combined effect physiological concentrations on hepatocytes remains unknown. Baicalin has been demonstrated to be antioxidant or chelator animal experiments. this study, we investigated injury CYP2E1-independently induced by combination protective baicalin. Compared with cells treated ethanol alone, ferric citrate enhanced accumulation reactive oxygen nitrogen species, increased occurrence protein carbonylation/nitration levels 4-hydroxy-2-nonenal, changed distribution iNOS, eventually resulted apoptosis. pretreatment baicalin inhibited iron, mainly chelating iron. Our findings therefore suggest that could CPY2E1-independently enhance alcohol, which probably contributes pathogenesis disease. a promising phytomedicine for preventing
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