It effectively abrogated the IL-1β-induced over-expression of inflammatory mediators by inhibiting the production of PGE2 and nitric oxide induced by IL-1β; in addition, it decreased the IL-1β-stimulated gene expression and production of MMP-3, MMP-13, iNOS, and COX-2 in human osteoarthritis chondrocytes; it also inhibited the IL-1β-mediated activation of NF-κB by suppressing the IκBα degradation in the cytoplasm [133]. This evidence concerns the gene IL1B and osteoarthritis.