ABSTRACT
Objective To study the protective effect of chlorogenic acid(CGA)on the apoptosis of PC12 cells induced byβ-amyloid protein23-35(Aβ25-35)and its mechanism. Methods The cells model of death was estab-lished by Aβ25-35 (20 μmol/L)-induced PC12 cells. The cells were interfered with 5 different concentrations of CGA. CCK-8 assay was used to detect cells viability to determine the 3 concentrations of CGA in future experi-ments. The cells were divided randomly into control group ,model group and interference groups with 3 different concentrations of CGA. Cells apoptosis rates were detected by flow cytometry;colorimetry method was used to detect MDA,SOD and GSH-Px. The mitochondrial membrane potential(MMP)was detected by fluorescent staining and the expression of caspase-3 by western blot. Results Compared with model group,the cells viability of CGA groups were increased but the apoptosis rates were reduced;the activity of SOD and GSH-Px were increased but the level of MDA,MMP and caspase-3 were decreased(P<0.05). Conclusions CGA has a protective effect on Aβ25-35-induced PC12 cells apoptosis and it may be related to the improvement of cellular antioxidation capacity and mitochondrial damage.