Protective effects of Schisandrin C on chondrocyte damage by inhibiting MAPK and NF-κB signal pathways

Abstract

Background: Osteoarthritis (OA) is a common joint disorder that affects the elderly population. The pathogenesis of OA is related to cartilage degradation and inflammatory response. Schisandrin C (Sch C), a dibenzocyclooctadiene derivative of Schisandra chinensis, has been demonstrated to exert anti-inflammatory effect in various inflammation diseases. However, the effect of Sch C on OA remains unclear. Thus, we aimed to investigate its action on chondrocytes and explore the mechanism associated with the inflammatory response. Methods: In this study, we chose rabbits and SW1353 cells as in vivo/in vitro models. Matrix metalloproteinase (MMP3), Nitric oxide (NO), IL-1β and TNF-α were detected by ELISA kits. The expression of MAPK/NF-κB related signaling molecules were determined by western blot. Results: In vitro, Sch C suppressed the IL-1β-induced production of NO and PGE2. Additionally, Sch C significantly decreased IL-1β-induced p65 phosphorylation and mitogen-activated protein kinase (MAPK) activation, as evidenced by the reduced phosphorylation of p38, extracellular signal-regulated kinase (ERK), and c-Jun amino-terminal kinase (JNK). Moreover, Sch C prevented cartilage damage in rabbit OA model with lower Mankin’s score than the model group. Sch C also inhibited the level of inflammatory cytokines in the articular cavity flushing fluid in rabbit OA model. Conclusions: Our study suggested that Sch C inhibited the IL-1β-induced inflammation and cartilage degradation through suppressing the MAPK and NF-κB signal pathways, indicating a potential in OA treatment.