BACKGROUND:Mechanical, inflammatory, and biochemical factors, particularly matrix metaloproteinases and reactive oxygen lead to chondrocyte degeneration in osteoarthritis. Curcumin has been shown to be a potent antioxidant; however, its protective effects against chondrocyte degeneration in osteoarthritis remain unclear.
OBJECTIVE:To investigate the potential molecular mechanisms underlying the protective effects of curcumin on articular cartilage of osteoarthritis in rats.
METHODS:A total of 30 Sprague-Dawley rats were used and randomly divided into model group (positive control,n=15) and normal group (negative control,n=15). Rat models of traumatic osteoarthritis were established, and then cartilage cels were isolated from articular cartilage and culturedin vitro. Chondrocytes were treated with curcumin (curcumin group) or PDTC (an inhibitor of nuclear factor-kappa B) for 24 hours. The expression level of nuclear factor-kappa B P65 in nucleus and cytoplasm in chondrocytes were determined by western blot assay and immunofluorescence. Moreover, mRNA expressions of type II colagen, matrix metaloproteinase-1 and -13 were analyzed using RT-qPCR.
RESULTS AND CONCLUSION: Nuclear factor-kappa B P65 protein was mainly expressed in nucleus, but few in cytoplasm in positive control group; the reversed results were found in the curcumin group. Nuclear translocation of nuclear factor-kappa B P65 was observed mainly in nucleus in the positive control group; however, that was observed mainly in cytoplasm in the negative control, curcumin, and PDTC groups. Matrix metaloproteinase-1 and -13 mRNA expressions were significantly decreased, while type II colagen mRNA expression was significantly increased in the curcumin group compared with the positive control group. These findings indicated that curcumin protect chondrocytes against degeneration through inhibiting the activation of nuclear factor-kappa B signaling pathway, suppressing nuclear translocation of nuclear factor-kappa B P65 and inhibiting the expressions of matrix metaloproteinase-1 and -13, which are responsible for upregulation of type II colagen expression.