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五味子乙素通过抑制NF-κB和MAPK信号通路改善软骨细胞炎症和骨关节炎。

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

作者信息

Ran Jisheng, Ma Chiyuan, Xu Kai, Xu Langhai, He Yuzhe, Moqbel Safwat Adel Abdo, Hu Pengfei, Jiang Lifeng, Chen Weiping, Bao Jiapeng, Xiong Yan, Wu Lidong

机构信息

Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

出版信息

Drug Des Devel Ther. 2018 May 9;12:1195-1204. doi: 10.2147/DDDT.S162014. eCollection 2018.

DOI:10.2147/DDDT.S162014
PMID:29785089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5953308/
Abstract

INTRODUCTION

Osteoarthritis (OA) is the most prevalent joint disorder in the elderly population, and inflammatory mediators like IL-1β were thought to play central roles in its development. Schisandrin B, the main active component derived from , exhibited anti-oxidative and antiinflammatory properties.

METHODS

In the present study, the protective effect and the underlying mechanism of Schisan-drin 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.

摘要

引言

骨关节炎(OA)是老年人群中最常见的关节疾病,白细胞介素-1β(IL-1β)等炎症介质被认为在其发展过程中起核心作用。五味子乙素是从五味子中提取的主要活性成分,具有抗氧化和抗炎特性。

方法

在本研究中,在体内和体外研究了五味子乙素对骨关节炎的保护作用及其潜在机制。

结果

结果表明,五味子乙素可降低IL-1β诱导的基质金属蛋白酶3(MMP3)、MMP13、IL-6和诱导型一氧化氮合酶(iNOS)的上调,并增加IL-1β诱导的II型胶原、聚集蛋白聚糖和Sox9的下调。五味子乙素显著降低IL-1β诱导的大鼠软骨细胞中p65磷酸化和p65核转位。丝裂原活化蛋白激酶(MAPK)的激活也受到五味子乙素的抑制,p38、细胞外信号调节激酶(Erk)和c-Jun氨基末端激酶(Jnk)磷酸化的减少证明了这一点。此外,五味子乙素可预防大鼠骨关节炎模型中的软骨退变,其Mankin评分显著低于对照组。

结论

我们的研究表明,五味子乙素通过抑制核因子-κB(NF-κB)和MAPK信号通路改善软骨细胞炎症和骨关节炎,表明其在骨关节炎治疗中具有潜在的治疗价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/8296dd57025d/dddt-12-1195Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/5e8db2b228fa/dddt-12-1195Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/e6665401863c/dddt-12-1195Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/94066f6e4765/dddt-12-1195Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/a7023cb7c388/dddt-12-1195Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/9ac16f29a105/dddt-12-1195Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/8296dd57025d/dddt-12-1195Fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/5e8db2b228fa/dddt-12-1195Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/e6665401863c/dddt-12-1195Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/94066f6e4765/dddt-12-1195Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/a7023cb7c388/dddt-12-1195Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/9ac16f29a105/dddt-12-1195Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0970/5953308/8296dd57025d/dddt-12-1195Fig6.jpg

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