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Aim:Oxidative stress plays a critical role in the pathogenic cascade leading to neuronal degeneration in AD.Consequently,the induction of endogenous antioxidative proteins by antioxidants seems to be a very reasonable strategy for delaying the disease’s progression.In previous work,we identified the neurotrophic and neuroprotective effects of geniposide,which result from the activation of glucagon-like peptide 1 receptor (GLP-1R).In this study,we explore the role of PI3 kinase sig-naling pathway in the neuroprotection of geniposide in PC12 cells.Methods: Cell viability was determined by MTr assay.Apoptosis was detected by Hoechst and PI double staining.The protein expression of Bcl-2 and phosphorylation of Akt308,Akt473,GSK-3β,and PDK1 was measured by West blot.Results: Geniposide induced the expression of the antiapoptotic protein Bcl-2,which inhibited apoptosis in PC12 cells induced by H2O2,and this effect could be inhibited by preincubation with LY294002,a selective inhibitor of PI3K.Further-more,geniposide enhanced the phosphorylation of Akt308,Akt473,GSK-3β and PDK1 under conditions of oxidative stress.Conclusion: These results demonstrate that the PI3K signaling pathway is involved in the neuroprotection of geniposide in PC12 cells against the oxidative damage induced by H202 in PC12 cells.