Therapeutic effects of triptolide from Tripterygium wilfordii Hook. f. on interleukin-1-beta-induced osteoarthritis in rats

Osteoarthritis (OA) is a common yet destructive disease affecting the articular cartilage, and is a major cause of immense suffering and disability for millions of people. Previous studies have shown that triptolide (TPL), an active compound derived from Tripterygium wilfordii, has potent immunosuppressive and anti-inflammatory activities useful for treating chronic diseases. However, whether TPL has immunosuppressive activity against OA is not known. In this study, we assessed the therapeutic effects of TPL on interleukin-1-beta (IL-1β)-induced OA in rats. Histological and protein analyses revealed that TPL not only could inhibit interleukin-6 (IL-6) and cyclooxygenase-2 (COX2) protein expression in cells and disrupt inflammation, but it also reduced the expression of matrix metalloproteinase (MMP)-3 and 13. Our results also supported the ability of TPL to suppress the osteoprotegerin/receptor activator of nuclear factor kappa-beta (NF-κB)/receptor activator of NF-κB ligand (OPG/RANK/RANKL) and NF-κB signaling pathways induced by IL-1β. Together these data suggest that TPL may be a potentially valuable treatment for OA, regulating associated inflammation and pain.

Keywords: IL-1β; NF-κB; OPG/RANK/RANKL; Osteoarthritis; Triptolide.