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

被引：77

作者：

Ran, Jisheng ^{[1
]}

Ma, Chiyuan ^{[1
]}

Xu, Kai ^{[1
]}

Xu, Langhai ^{[1
]}

He, Yuzhe ^{[1
]}

Moqbel, Safwat Adel Abdo ^{[1
]}

Hu, Pengfei ^{[1
]}

Jiang, Lifeng ^{[1
]}

Chen, Weiping ^{[1
]}

Bao, Jiapeng ^{[1
]}

Xiong, Yan ^{[1
]}

Wu, Lidong ^{[1
]}

机构：

[1] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Orthoped Surg, 88 Jiefang Rd, Hangzhou 310000, Zhejiang, Peoples R China

来源：

DRUG DESIGN DEVELOPMENT AND THERAPY | 2018年 / 12卷

基金：

中国国家自然科学基金;

关键词：

osteoarthritis; Schisandrin B; chondrocytes; MMPs; NF-kappa B pathway; MAPK pathway; TUMOR-NECROSIS-FACTOR; MATRIX METALLOPROTEINASES; LIFETIME RISK; CARTILAGE; DEGRADATION; INHIBITION; ACTIVATION; RESPONSES;

D O I：

10.2147/DDDT.S162014

中图分类号：

R914 [药物化学];

学科分类号：

100705 [微生物与生化药学];

摘要：

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.

引用

页码：1195 / 1204

页数：10

共 28 条

[1]

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