4.5 Article

Thymoquinone Inhibits IL-1β-Induced Inflammation in Human Osteoarthritis Chondrocytes by Suppressing NF-κB and MAPKs Signaling Pathway

Journal

INFLAMMATION
Volume 38, Issue 6, Pages 2235-2241

Publisher

SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-015-0206-1

Keywords

thymoquinone; osteoarthritis chondrocyte; IL-1 beta; NF-kappa B

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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(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(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.

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