Protective Effect of Icariin on H₂O₂-induced Chondrocyte Oxidative Damage and Its Mechanism

OBJECTIVE To explore the protective effect of icariin(ICA) on H₂O₂-induced chondrocyte oxidative damage and its related mechanism. METHODS SD neonatal rat chondrocytes were isolated and randomly divided into control group, H₂O₂ model group, ICA low dose group, ICA medium dose group and ICA high dose group. CCK8 assay was used to detect the change of cell proliferation ability in each group. The expression of reactive oxygen(ROS), superoxide dismutase(SOD), malondialdehyde(MDA), catalase(CAT) and glutathione peroxidase(GSH-Px) in each group were detected by ELISA kit. Cell cycle of each group was detected by flow cytometry and proliferation index(PI) was calculated. Hoechst staining was used to observe the cell apoptosis in each group. qRT-PCR and Western blotting were used to detect the expression of apoptosis related factors and Nrf2/HO-1 pathway. RESULTS Compared with the control group, the proliferation ability of cells in the H₂O₂ model group was decreased, ROS and MDA contents were increased, SOD, CAT and GSH-Px contents were decreased, and cell apoptosis was increased. After ICA intervention, the proliferation ability of chondrocytes increased, ROS and MDA contents decreased, SOD, CAT and GSH-Px contents increased, and ICA could effectively inhibit chondrocyte apoptosis and up-regulate the expression of Nrf2 and HO-1 proteins. CONCLUSION ICA has a protective effect on H₂O₂-induced oxidative damage of chondrocytes and can inhibit chondrocyte apoptosis, and the mechanism is related to Nrf2/HO-1 pathway.