Gossypin Protect against Cartilage Injury via Reduction of Pro-inflammatory Cytokines and Modulation of Cartilage Related Gene in Monosodium Iodoacetate Induced Osteoarthritic Rats

Osteoarthritis (OA), a heterogeneous condition, leads to deformity in the joints and causes defects in the articular cartilage thereby inducing changes in the bone-joint margins. In this study, we studied the anti-osteoarthritic activity of gossypin against the monosodium iodoacetate (MIA)-induced osteoarthritis and explored the possible mechanism of action of gossypin. MIA (3 mg/50 mu L) was used to induce OA in the rats. Animals were divided into seven groups and were administered with different doses of gossypin (25, 50, and 100 mg/kg) and celecoxib (60 mg/kg). Body weight and joint formation were estimated at regular intervals. At end of the study, proinflammatory cytokines, inflammatory mediators, and the expression of matrix metalloproteinases (MMPs) such as MMP-2, MMP-3, MMP-9, and MMP-13; tissue inhibitors of metalloproteinases (TIMPs); and collagen type II (COL2) were measured in the serum. Administration of gossypin significantly increased the body weight and organ weight (liver, heart, spleen, and heart) and reduced the diameter of the joint (p < 0.001). Gossypin significantly decreased the levels of pro-inflammatory cytokines and inflammatory mediators. Italso downregulated the expression of MMP-2, MMP-3, MMP-9, and MMP-13 and upregulatedthe expression of TIMPs and COL2. Gossypin down-regulated the mRNA expression of MMP and upregulated the expression of TIMP and COL2 byreducing the proinflammatory cytokines and inflammatory mediators.