OBJECTIVE：To study the protective effects of butein on oxidative stress injury of PC12 cell and its effects on mitochondrial function. METHODS：Rats PC12 cells were divided into normal control group，model group，solvent control group（1 ‰ dimethyl sulfoxide），butein high，medium and low concentration groups（2，1，0.5 μmol/L）. The latter 4 groups were given relevant reagent/medicine for intervention；24 h later，other groups were given 100 mU/mL glucose oxidase to induce oxidant stress model except for normal control group. After 4 h culture，cell survival rate，apoptosis rate，the levels or activities of ROS，MDA，SOD，CAT，GSH-Px，ATP，IL-1β and TNF-α as well as the change of MMP were detected. RESULTS：Compared with normal control group，cell survival rate，the levels or activities of SOD，CAT，GSH-Px and ATP were all decreased significantly，and apoptotic rate，the content of ROS，the levels of MDA，IL-1β and TNF-α were all increased significantly（P＜0.05 or P＜0.01），while the MMP was decreased significantly. Compared with model group，above indexes of solvent control group had no significant change （P＞0.05），cell survival rates，the levels or activities of SOD （except for medium and low concentration groups），CAT，GSH-Px（except for medium and low concentration groups），ATP（except for low concentration group）were increased significantly in butein high，medium and low concentration groups，while apoptotic rates，the content of ROS，the levels of MDA，IL-1 β and TNF-α were decreased significantly（P＜0.05 or P＜0.01），while the MMP were increased significantly. CONCLUSIONS：Butein can increase the antioxidant enzyme activity， stabilize mitochondrial function， inhibit oxidative stress and inflammationthus， increase energy generation inhibiting neuronal cell apoptosis ultimately exerting a neuroprotective effect.