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