OBJECTIVE： To study the effects of aripiprazole on PC12 cell injury induced by amyloid β-protein （Aβ25-35） and its mechanism. METHODS： PC12 cells were randomized into normal control group， model group （20 μmol/L Aβ25-35）， aripiprazole low-concentration， medium-concentration and high-concentration groups （5， 10， 20 μmol/L aripiprazole+20 μmol/L Aβ25-35）. These groups were cultured with culture medium containing relevant medicine for 48 h， with 6 wells in each group. The viability （optical density value） of PC12 cell was measured by MTT assay， and PC12 cell apoptosis was measured by Hoechst staining. The activities of Caspase-3 and Caspase-9 were determined by spectrophotometry. The protein expression of Bcl-2， Bax and PI3K and the phosphorylation of Akt were assayed by Western blot assay. RESULTS： Compared with normal control group， optical density value of model group was decreased while apoptotic rate was increased； the activities of Caspase-3 and Caspase-9， and the protein expression of Bax were increased； the protein expression of Bcl-2 and PI3K， the phosphorylation of Akt were decreased （P＜0.01）. Compared with model group， optical density value of aripiprazole low-concentration， medium-concentration and high-concentration groups were increased， while apoptotic rate and the activities of Caspase-3 and Caspase-9 were decreased； the protein expression of Bcl-2 and PI3K and the phosphorylation of Akt were enhanced； while the protein expression of Bax were decreased in aripiprazole medium-concentration and high-concentration groups （P＜0.05 or P＜0.01）. CONCLUSIONS： Aripiprazole can suppress cell apoptosis of PC12 cell induced by Aβ25-35， which is related to activating PI3K/Akt signal pathway.