Investigation of apoptosis mechanism in chondrocytes for prevention of osteoarthritis

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Objective: Oxidative stress has been reported to induce apoptosis and degeneration of chondrocytes.But the mechanism of EPA in apoptosis and degeneration of chondrocytes has been unknouwn. We evaluated that the function of EPA on apoptosis and degeneration of chondrocytes.Methods: The expression of MMPs were detected by real-time PCR, and apoptosis related proteins were detected by western blotting and FACS. C57BL/6J mice were used for detecting MMPs expression by immunohistochemistry.Results: EPA inhibited SNP-induced apoptosis of chondrocytes. EPA inhibited SNP-induced expressions of MMP3 and MMP13. The progression of OA was prevented by articular injection of EPA in vivo. Immunohistochemistry demonstrated that MMP3 and MMP13 expression were increased in DMM model. However, intra-articular injection of EPA inhibited the expressions of MMP13. Conclusion: The treatment of EPA can control the oxidative stress-induced OA progression. EPA may be a new therapeutic approach in OA therapy.