Anti-chondrocyte apoptosis effect of genistein in treating inflammation-induced osteoarthritis

Osteoarthritis (OA) is a chronic disease that is mainly characterized by chondrocyte degeneration. Inflammatory mediators participate in the development of OA, leading to chondrocyte apoptosis and destruction of the cartilage. Genistein is the major active component of isoflavone, with a chemical composition and a biological effect that is similar to that of estrogens, which prevents the degradation of cartilage; however, its underlying mechanisms of action remain unknown. The aim of the present study was to investigate the anti-apoptotic effects of genistein on chondrocytes for the treatment of inflammation-induced OA. Interleukin (IL)-1β was used to establish a chondrocyte OA model. After treatment with different concentrations of genistein, western blotting identified that expression levels of collagen II and aggrecan were increased in a concentration-dependent manner, while caspase 3 expression gradually decreased after genistein application. Moreover, flow cytometry and ELISA results demonstrated that genistein could decrease chondrocyte apoptosis and reduce the levels of tumor necrosis factor (TNF)-α in a dose-dependent manner. Furthermore, the in vitro data were evaluated in an OA rat model. Genistein increased the collagen and acid glycosaminoglycan content, as well as decreased the levels of TNF-α and IL-1β. Genistein also promoted the expression levels of collagen II and aggrecan in the articular cartilage, and decreased the expression of caspase 3, thus alleviating cartilage degradation. In conclusion, the results indicated that genistein mediated inflammation and had an anti-apoptotic role in treating OA. Therefore, genistein may serve as an alternative treatment for OA.