Ginsenoside Ro suppresses interleukin-1β-induced apoptosis and inflammation in rat chondrocytes by inhibiting NF-κB

This study investigated effects of Ginsenoside Ro (Ro) on interleulcin-1 beta (IL-1 beta)-induced apoptosis and inflammation in rat chondrocytes. The rat chondrocytes were co-treated with IL-1 beta (10 ng.kg(-1)) and Ro (50, 100 and 200 mu mol.L-1) for 48 h. Choudrocytes viability was detected by the MTT assay and Annexin V-FITC/PI dual staining assay. Caspase 3 activity was measured by using caspase 3 colorimetric assay kit. Apoptosis related proteins Box, Bad, Bcl-x(L), PCNA, p53 and phospho-p53, along with inflammation related protein NIMP 3, MNIP 9 and COX-2, and the expression of phospho-NF-kappa B p65 were assayed by western blotting analyses. Ro could improve IL-1 beta-induced chondrocytes viability. Ro could suppress IL-1 beta-induced apoptosis by inhibiting levels of Bax and Bad, decreasing p53 phosphorylation and promoting the expression of Bcl-x(L) and PCNA. Ro inhibited caspase 3 activity. IL-1 beta-induced inflammation and matrix degration were also alleviated by Ro with down-regulating the expression of MMP 3, MMP 9 and COX-2. Moreover, Ro inhibited NF-kappa B p65 phosphorylation induced by IL-1 beta In conclusion, these results suggested Ro exerted anti-apoptosis and anti-inflammation in IL-1 beta-induced rat chondrocytes, which might be related to NF-kappa B signal pathway. Therefore, we propose that Ro might be a potential novel drug for the treatment of osteoarthritis.