Thymoquinone Inhibits IL-1[beta]-Induced Inflammation in Human Osteoarthritis Chondrocytes by Suppressing NF-[kappa]B and MAPKs Signaling Pathway

• Published in: Inflammation 2015-12, Vol.38 (6), p.2235
• Main Authors: Wang, Dongyan, Qiao, Jiutao, Zhao, Xin, Chen, Tianxin, Guan, Dehong
• Format: Article
• Language: English
• ISSN: 0360-3997; 1573-2576
• DOI: 10.1007/s10753-015-0206-1

Thymoquinone, an active ingredient isolated from Nigella sativa, has been reported to have anti-inflammatory effects. However, the anti-inflammatory effect of thymoquinone on IL-1[beta]-stimulated osteoarthritis chondrocytes remains unclear. In this study, we designed to investigate the anti-inflammatory effects and elucidated the underlying mechanism of thymoquinone on IL-1[beta]-stimulated human osteoarthritis chondrocytes. The effects of thymoquinone on inflammatory mediators COX-2, iNOS, NO, PGE^sub 2^, as well as MMP-1, MMP3, MMP13 production were detected. The results demonstrated that thymoquinone concentration-dependently inhibited IL-1[beta]-induced COX-2, iNOS, NO, and PGE^sub 2^ production. Thymoquinone also suppressed IL-1[beta]-induced MMP-1, MMP3, and MMP13 production. We found that thymoquinone significantly inhibited IL-1[beta]-induced NF-[kappa]B activation and I[kappa]B[alpha] degradation. In addition, thymoquinone was found to suppress IL-1[beta]-induced mitogen-activated protein kinases (MAPKs) activation. In conclusion, thymoquinone inhibited IL-1[beta]-induced inflammatory mediator production by inhibition of NF-[kappa]B and MAPKs signaling pathways in osteoarthritis chondrocytes. Thymoquinone may be a potential agent in the treatment of osteoarthritis.