Oridonin inhibits IL-1β-induced inflammation in human osteoarthritis chondrocytes by activating PPAR-γ

被引：26

作者：

Jia, Tao ^{[1
]}

Cai, Mengmeng ^{[1
]}

Ma, Xu ^{[1
]}

Li, Ming ^{[1
]}

Qiao, Jiutao ^{[1
]}

Chen, Tianxin ^{[1
]}

机构：

[1] Harbin Med Univ, Affiliated Hosp 2, Dept Orthopaed Surg, Harbin 150086, Heilongjiang, Peoples R China

来源：

INTERNATIONAL IMMUNOPHARMACOLOGY | 2019年 / 69卷

关键词：

Oridonin; Chondrocytes; IL-1; beta; NF-kappa B; NF-KAPPA-B; SYNOVIAL FIBROBLASTS; RECEPTOR; CYTOKINES; CELLS; PROGRESSION; CARTILAGE; AGONIST;

D O I：

10.1016/j.intimp.2019.01.049

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Osteoarthritis (OA), a progressive disease of the joints, affects millions of people worldwide. In the present study, we investigated the effects of oridonin, a diterpenoid isolated from Rabdosia rubescens, on IL-1 beta-induced inflammation using human osteoarthritis chondrocytes. The results showed that oridonin significantly suppressed IL-1 beta-induced MMP1, MMP3, and MMP13 production. IL-1 beta-induced NO and PGE(2) production, as well as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression were also attenuated by oridonin. Western blot analysis demonstrated IL-1 beta-induced NF-kappa B activation was reduced by oridonin. Furthermore, the expression of PPAR-gamma was increased by oridonin in a concentration-dependent manner. PPAR-gamma antagonist could reverse the anti-inflammatory activity of oridonin. The results suggested that oridonin could be a candidate agent for the treatment of OA.

引用

页码：382 / 388

页数：7

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