Objective: To establish a model of oxidative injury of Parkinson’s disease with PC12 cells treated b y 6-OHDA. To study the protective effect of GM1 on oxidative stress injury and potential mechanism involved . Methods : Cells were divided into control group and treated groups at random. Control group was maintained in normal medium; treated groups were exposed to 120μmol/L 6-OHDA with different concentrations of GM1 and 50 μmol/L LY294002. The MTT assay was used to evaluate the viability of PC12. The level of ROS was detected by staining cells with DCFH-DA. The contents of MDA and Na+K+ATPase were also determined. The apoptotic ratio was determined by flow cytometry (FCM). Result: In compare with that of cell treated by 6-OHDA only, the viability of cell treated by GM1 was added, and Na+K+ATPase activity was recovered with the concentrations of NGF increasing. The levels of ROS and MDA were lower in groups treated by GM1 than control. Conclusion GM1 have the protective effect on oxidative stress injury in PC12 cell induced by 6-OHDA. The Protective Effect of GM1 on oxidative stress of Parkinson’s Disease may rely on the activation of PI3-K/Akt and Nrf2 pathway.