Effects of Aripiprazole on PC12 Cell Injury Induced by Aβ25-35 and Its Mechanism / 中国药房

ABSTRACT

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 activi-ties 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 expres-sion of Bax were increased;the protein expression of Bcl-2 and PI3K,the phosphorylation of Akt were decreased(P<0.01). Com-pared 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 apop-tosis of PC12 cell induced by Aβ25-35,which is related to activating PI3K/Akt signal pathway.