Echinocystic Acid Inhibits IL-1[beta]-Induced COX-2 and iNOS Expression in Human Osteoarthritis Chondrocytes

Echinocystic acid (EA), a pentacyclic triterpene isolated from the fruits of Gleditsia sinensis Lam, displays a range of pharmacological activities including anti-inflammatory and antioxidant effects. However, the effect of EA on IL-1[beta]-stimulated osteoarthritis chondrocyte has not been reported. The purpose of this study was to assess the effects of EA on IL-1[beta]-stimulated human osteoarthritis chondrocyte. Chondrocytes were stimulated with IL-1[beta] in the absence or presence of EA. NO and PGE^sub 2^ production were measured by Griess reagent and ELISA. The expression of COX-2, iNOS, nuclear factor-[kappa]B (NF-[kappa]B), inhibitory kappa B (I[kappa]B[alpha]), c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK) were detected by Western blot analysis. The results showed that EA suppressed IL-1[beta]-induced collagenase-3 (MMP-13), NO, and PGE^sub 2^ production in a dose-dependent manner. IL-1[beta] up-regulated the expression of COX-2 and iNOS, and the increase was inhibited by EA. Furthermore, IL-1[beta]-induced NF-[kappa]B and mitogen-activated protein kinase (MAPK) activation were inhibited by EA. In conclusion, EA effectively attenuated IL-1[beta]-induced inflammatory response in osteoarthritis chondrocyte which suggesting that EA may be a potential agent in the treatment of osteoarthritis.