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Inflammation
Published in: Inflammation 4/2016

01-08-2016 | ORIGINAL ARTICLE

Coptisine Prevented IL-β-Induced Expression of Inflammatory Mediators in Chondrocytes

Authors: Kai Zhou, Li Hu, Wenjun Liao, Defeng Yin, Feng Rui

Published in: Inflammation | Issue 4/2016

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Abstract

Interleukin 1β (IL-1β) is a pleiotropic pro-inflammatory cytokine that plays a critical role in the development of osteoarthritis (OA). Coptisine is an isoquinoline alkaloid extracted from Coptidis rhizome and has been reported to possess anti-inflammatory activity. However, the anti-inflammatory effects of coptisine on interleukin-1 beta (IL-1β)-stimulated chondrocytes have not been reported. Therefore, the aim of this study was to investigate the effects of coptisine on IL-1β-induced inflammation in human articular chondrocytes. Our results showed that coptisine greatly inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2), as well as suppressed the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in human OA chondrocytes induced by IL-1β. It also inhibited the expression of matrix metalloproteinase-3 (MMP-3) and MMP-13 in IL-1β-stimulated human OA chondrocytes. Furthermore, coptisine significantly inhibited the IL-1β-induced NF-kB activation in human OA chondrocytes. Taken together, these data suggest that coptisine inhibits the IL-1β-induced inflammatory response by suppressing the NF-kB signaling pathway. Thus, coptisine may be a potential agent in the treatment of OA.
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Metadata
Title
Coptisine Prevented IL-β-Induced Expression of Inflammatory Mediators in Chondrocytes
Authors
Kai Zhou
Li Hu
Wenjun Liao
Defeng Yin
Feng Rui
Publication date
01-08-2016
Publisher
Springer US
Published in
Inflammation / Issue 4/2016
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-016-0391-6

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