Ginsenoside-Rb1 inhibits monoiodoacetate-induced osteoarthritis in postmenopausal rats through prevention of cartilage degradation

Background Ginsenoside Rb1 (G-Rb1), one of the major active compounds in Panax ginseng, has already been shown to reduce inflammation in various diseases. Osteoarthritis (OA) has traditionally been considered a degenerative disease with degradation of joint articular cartilage. However, recent studies have shown the association of inflammation with OA. In the present study, we investigated whether Rb1 had an anti-inflammatory effect on monoiodoacetate (MIA)-induced OA in ovariectomized rats as a model of postmenopausal arthritis. Methods G-Rb1 at a dosage of 3 and 10 μg/kg body weight was administered every 3 days intra-articularly for a period of four weeks to observe anti-arthritic effects. Diclofenac (10 mg/kg) served as a positive control. Results The administration of Rb1 significantly ameliorated OA inflammatory symptoms and reduced serum levels of inflammatory cytokines. Furthermore, G-Rb1 administration considerably enhanced the expression of bone morphogenetic protein-2 and collagen 2A and reduced the levels of matrix metalloproteinase-13 genes, indicating a chondro-protective effect of G-Rb1. G-Rb1 also significantly reduced the expression of several inflammatory cytokines/chemokines (IFN-γ, MCP-1/CCL-2, IL-1β, and IL-6). Histological analysis demonstrated that G-Rb1 significantly attenuated the pathological changes in MIA-induced OA in ovariectomized rats. Safranin O and toluidine blue staining further demonstrated that G-Rb1 effectively prevented the degradation of cartilage and glycosaminoglycans, respectively. Conclusion Overall, our results suggest that G-Rb1 exerts cartilage protective effect on MIA induced ovariectomized OA rats, by inhibiting inflammatory mediators such as IL-6, IL-1β, MCP1/CCL2, COX-2, and PGE2. These results shed a light on possible therapeutic application of G-Rb1 in OA.