Carvacrol ameliorates inflammatory response in interleukin 1β-stimulated human chondrocytes.

Abstract

Carvacrol, a monoterpenic phenol present in Origanumvulgare (oregano) and Thymusvulgaris (thyme), possesses anti‑inflammatory effects; however, little is known about the effects and underlying mechanism of carvacrol on chondrocytes in osteoarthritis (OA). The present study aimed to investigate the protective effects of carvacrol against inflammation in interleukin 1β (IL‑1β)‑stimulated human chondrocytes. The results indicated that carvacrol inhibited nitric oxide (NO) and prostaglandin E2 (PGE2) production, and decreased the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX‑2). Carvacrol also suppressed the protein expression levels of matrix metalloproteinase (MMP)‑3 and MMP‑13 in IL‑1β‑stimulated human OA chondrocytes. Furthermore, carvacrol suppressed the activation of nuclear factor (NF)‑κB signaling pathway in IL‑1β‑induced human chondrocytes. In conclusion, the present results demonstrated that carvacrol was able to inhibit IL‑1β‑induced NO and PGE2 production, as well as iNOS, COX‑2 and MMPs expression in human chondrocytes by suppressing the activation of NF‑κB signaling pathway. Thus, carvacrol may have potential therapeutic functions for the treatment of OA.