ABSTRACT
Objective To explore the protective effects of quercetin on damage induced by oxidative stress and to clari?fy its molecular mechanism. Methods Chang liver cell cultures were randomly divided into control groups, H2O2 group and 3 doses of quercetin groups. Cell survival rate was detected with MTT. Cell apoptotic rate was measured by FACS(Fluores?cence-activated cell sorting). Intracellular reactive oxygen species (ROS) level in Chang liver cells were tested by flow cy?tometer. The DCF fluorescence intensity of DCFH-DA-stained intracellular ROS was observed by fluorescence microscope. The levels of malondialdehyde (MDA), superoxide dismutase(SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were determined in liver cells using commercial available kits. The expression of Nrf2 were detected by Western blot. Re?sults Compared with control, cell survival rate and levels of SOD, CAT and GSH-Px decreased significantly in H2O2 group (P < 0.05 ),while cell appotosis rate, content of MDA and mean fluorescence intensity(MFI) increased in H2O2 group (P <0.05). In comparison with H2O2, expression of Nrf2 protein was higher in all three quercetin treatment groups (P<0.05). Con?clusion Quercetin protected Chang liver cells from H2O2-induced oxidative stress, which may be caused by the increased ex?pressions of down stream antioxidant genes via activating the Nrf2-ARE signaling pathway.