Isofraxidin inhibits interleukin-1β induced inflammatory response in human osteoarthritis chondrocytes

被引：33

作者：

Lin, Jian

Li, Xiaobin

Qi, Weihui

Yan, Yingzhao

Chen, Kai

Xue, Xinghe

Xu, Xinxian

Feng, Zhenhua

Pan, Xiaoyun ^{[1
,2
]}

机构：

[1] Wenzhou Med Univ, Affiliated Hosp 2, Dept Orthopaed, Wenzhou 325000, Zhejiang, Peoples R China

[2] Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou 325000, Zhejiang, Peoples R China

来源：

INTERNATIONAL IMMUNOPHARMACOLOGY | 2018年 / 64卷

关键词：

Osteoarthritis; Inflammation; Isofraxidin; Chondrocytes; NF-kappa B; FACTOR-KAPPA-B; TUMOR-NECROSIS-FACTOR; TNF-ALPHA; ACANTHOPANAX-SENTICOSUS; COUMARIN COMPONENT; MATRIX DEGRADATION; INDUCED APOPTOSIS; GENE-EXPRESSION; CARTILAGE; PATHWAY;

D O I：

10.1016/j.intimp.2018.09.003

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) is the most prevalent disease of knee especially in the aged people. Isofraxidin (IF) is a coumarin compound refined from traditional Chinese medicines with potential anti-inflammatory ability. This study aimed to evaluate protective anti-inflammatory effects of IF in human OA chondrocytes. The chondrocytes were isolated from OA patients and pretreated with IF before treatment with IL-1 beta. The results showed that IF blocked IL-1 beta-stimulated production of NO and PGE2. In addition, IF inhibited the expression of COX-2, iNOs, MMP-1, MMP-3, MMP-13, ADAMTS-4 and ADAMTS-5, and increased the levels of aggrecan and collagen-II. Mechanistically, IF suppressed IL-1 beta-induced I kappa B-alpha degradation and NF-kappa B activation. In conclusion, our results demonstrate that IF inhibits inflammation in OA via the regulation of NF-kappa B signaling, and suggest that IF may be a potential therapeutic agent for OA.

引用

页码：238 / 245

页数：8

共 42 条

[11]

2-1

[12] Induction of an Inflammatory and Prodegradative Phenotype in Autologous Fibroblast-like Synoviocytes by the Infrapatellar Fat Pad From Patients With Knee Osteoarthritis [J].