Oxymatrine ameliorates osteoarthritis via the Nrf2/NF-κB axis in vitro and in vivo

Osteoarthritis (OA) is a common degenerative joint disorder. Currently, the underlying etiology of OA is still far from fully elucidated and there is no cure for OA progression. Previous studies have demonstrated that oxymatrine (OMT) could inhibit inflammation and oxidative stress in several animal models. However, the potential effects of OMT on OA remain largely elusive. The aim of the study is to investigate the anti-inflammatory and chondrocyte protective effect of OMT, and delineate the potential mechanism in vitro and in vivo.Western blotting, RT-PCR, ELISA and tissue staining were employed to explore the mechanisms by which OMT exerted a protective effect on IL-1β-induced production of pro-inflammation cytokines and extracellular matrix (ECM) degradation in primary murine chondrocytes and DMM mouse models.The results showed that OMT reduced the IL-1β-induced over-production of pro-inflammation cytokines and ECM degradation. Mechanistically, OMT inhibited the NF-κB pathway via activating Nrf2. In vivo studies also demonstrated that OMT ameliorated OA progression.OMT reduced pro-inflammation cytokines, ECM degradation and OA progression via activating Nrf2 and inhibiting NF-κB pathway.