Leonurine inhibits IL-1β induced inflammation in murine chondrocytes and ameliorates murine osteoarthritis

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by cartilage degradation, subchondral bone sclerosis and synovitis. Leonurine, an active component extracted from the leaves of Herba leonuri, has been reported to possess various potent biological effects such as anti-oxidant, anti-apoptosis, and anti-inflammatory. However, the therapeutic benefits of leonurine on OA have not been reported. This study aimed to evaluate the therapeutic effect of leonurine on chondrocytes and in murine OA models. Murine chondrocytes were pre-treated with leonurine (5, 10, and 20 μM) for 2 h and then stimulated with IL-1β for 24 h. Production of NO, PGE2, IL-6, TNF-α, MMP-3, MMP-13, and ADAMTS-5 was assessed with the Griess reagent and ELISAs. The mRNA expression of COX-2, iNOS, MMP-3, MMP-13, ADAMTS-5, aggrecan, and collagen-II was tested with real-time polymerase chain reaction. The protein expression of iNOS, COX-2 and NF-κB-related signaling molecules was measured with western blotting. In this study, leonurine visibly inhibited the IL-1β-induced production of NO, PGE2, IL-6 and TNF-α; and decreased the expression of iNOS, COX-2, MMP-3, MMP-13 and ADAMTS-5 in chondrocytes. Furthermore, leonurine significantly suppressed IL-1β-stimulated NF-κB activation. In addition, treatment with leonurine not only prevented cartilage destruction and subchondral bone thickening, but also alleviated synovitis in a murine OA model. Taken together, these results suggest that leonurine may be a potential therapeutic agent in OA treatment. •Leonurine inhibited IL-1β-induced pro-inflammatory cytokines expression in chondrocytes.•Chondrocytes degradation and NF-κB activation were both inhibited by leonurine treatment.•Leonurine may be a potential therapeutic agent in OA treatment.