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

被引:31
|
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
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
收藏
页码:238 / 245
页数:8
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