[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, H2O2 group, CGA + H2O2 group, 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 H2O2 group, 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.