Mechanism of chlorogenic acid on apoptosis of rat nucleus pulposus cells induced by oxidative stress

Objective: To investigate the mechanism of chlorogenic acid(CGA) on H2O2-induced apoptosis in the rat nucleus pulposus cells(NPCs). Methods: NPCs were isolated from SD rats and cultured in vitro. Cultured cells(P3) were randomly divided into normal control group,H2O2group,CGA + H2O2group,CGA group and LY294002 pretreatment group. The apoptosis and ROS production of rNPCs was detected by flow cytometry. The expressions of p-Akt,BCL-2 and Akt were analyzed by Western blot. Results: Compared with normal control group,in the H2O2group,the production of ROS and the apoptosis rate significantly increased in rNPCs; CGA treatment inhibited ROS production and cell apoptosis,while increased the expression of p-Akt and BCL-2; LY294002,a PI3Kinse inhibitor,not only decreased the expression of p-Akt and BCL-2,but also obviously increased ROS production and cell apoptosis. Conclusion: Chlorogenic acid can protect NPCs against apoptosis by oxidative stress through decreasing reactive oxygen species production and increasing anti-apoptotic protein BCL-2 expression in NPCs by activation of PI3K-Akt signaling pathways.