Schisandrin B ameliorated chondrocytes inflammation and osteoarthritis via suppression of NF-κB and MAPK signal pathways

Introduction: Osteoarthritis (OA) is the most prevalent joint disorder in the elderly population, and inflammatory mediators like IL-1 beta were thought to play central roles in its development. Schisandrin B, the main active component derived from Schisandra chinensis, exhibited antioxidative and antiinflammatory properties. Methods: In the present study, the protective effect and the underlying mechanism of Schisandrin B on OA was investigated in vivo and in vitro. Results: The results showed that Schisandrin B decreased IL-1 beta-induced upregulation of matrix metalloproteinase 3 (MMP3), MMP13, IL-6, and inducible nitric oxide synthase (iNOS) and increased IL-1 beta-induced downregulation of collagen II, aggrecan, and sox9 as well. Schisandrin B significantly decreased IL-1 beta-induced p65 phosphorylation and nuclear translocation of p65 in rat chondrocytes. Mitogen-activated protein kinase (MAPK) activation was also inhibited by Schisandrin B, as evidenced by the reduction of p38, extracellular signal-regulated kinase (Erk), and c-Jun amino-terminal kinase (Jnk) phosphorylation. In addition, Schisandrin B prevented cartilage degeneration in rat OA model with significantly lower Mankin's score than the control group. Conclusion: Our study demonstrated that Schisandrin B ameliorated chondrocytes inflammation and OA via suppression of nuclear factor-kappa B (NF-kappa B) and MAPK signal pathways, indicating a therapeutic potential in OA treatment.