期刊
DRUG DESIGN DEVELOPMENT AND THERAPY
卷 12, 期 -, 页码 1195-1204出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/DDDT.S162014
关键词
osteoarthritis; Schisandrin B; chondrocytes; MMPs; NF-kappa B pathway; MAPK pathway
资金
- National Natural Science Foundation of China [81371996, 81572173]
- Natural Science Foundation of Zhejiang Province [LQ18H060001]
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.
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