RESUMO
Curcumin possesses strong anti-inflammatory, anti-rheumatoid and anti-oxidative activities, and has the potential to inhibit nuclear factorκB (NFκB) signaling. Cartilage damage in osteoarthritis (OA) is largely mediated by interleukin-1ß (IL-1ß) via activation of various transcription factors, including NFκB and activator protein1. The aim of the present study was to determine whether IL1ß induces matrix metalloproteinase-13 (MMP-13) expression and inhibits type II collagen expression, as well as to examine whether cell proliferation may be inhibited by curcumin through the inhibition of NFκB signaling. The effects of curcumin were investigated in rat articular chondrocyte cell cultures treated with IL1ß in the presence or absence of curcumin or the NFκB inhibitor pyrrolidine dithiocarbamate. Western blotting and reverse transcriptionquantitative polymerase chain reaction were conducted to evaluate protein and mRNA expression levels of type II collagen, MMP13, NFκB inhibitor α (IκBα), phosphorylatedIκBα and NFκB subunit p65/RelA. Western blotting and immunofluorescence were performed to examine the effects of curcumin on the expression, phosphorylation and nuclear translocation of NFκBassociated proteins. The effects of curcumin on cell proliferation were evaluated by Cell Counting Kit8 (CCK8). Curcumin was demonstrated to inhibit the IL1ßinduced activation of NFκB by suppressing IκBα phosphorylation and p65/RelA nuclear translocation. These events were associated with the downregulation of MMP13 expression and the upregulation of type II collagen expression, both of which are considered to be NFκB targets. CCK8 assays revealed that cotreatment with curcumin resulted in increased proliferation in IL1ßtreated chondrocytes. These findings implicated curcumin as a naturally occurring antiinflammatory agent for the treatment of OA via inhibition of NFκB signaling.