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

Jisheng Ran,* Chiyuan Ma,* Kai Xu,* Langhai Xu, Yuzhe He, Safwat Adel Abdo Moqbel, Pengfei Hu, Lifeng Jiang, Weiping Chen, Jiapeng Bao, Yan Xiong, Lidong Wu Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China *These authors contributed equally to this work Introduction: Osteoarthritis (OA) is the most prevalent joint disorder in the elderly population, and inflammatory mediators like IL-1βwere 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-1β-induced upregulation of matrix metalloproteinase 3 (MMP3), MMP13, IL-6, and inducible nitric oxide synthase (iNOS) and increased IL-1β-induced downregulation of collagen II, aggrecan, and sox9 as well. Schisandrin B significantly decreased IL-1β-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-κB (NF-κB) and MAPK signal pathways, indicating a therapeutic potential in OA treatment. Keywords: osteoarthritis, Schisandrin B, chondrocytes, MMPs, NF-κB pathway, MAPK pathway