［Objective］ To investigate the effect of miR-145 on autophagy and chondrocyte viability under oxidative stress by regulating FRS2 （Fibroblast Growth Factor Receptor Substrate 2）expression. ［Methods］ Eight week old male C57 mice were reared adaptively for 7 days. The OA model was established by medial meniscus instability induction. Two weeks later, the mice were killed. Safranin O staining was used to detect the cartilage damage in mice. Immunohistochemistry was used to detect the expression of FRS2, LC3 I / II and p62. The results showed that miR-145 could protect the articular cartilage of osteoarthritis mice by inhibiting FRS2 induced autophagy. ［Results］ After successful modeling, autophagy related markers in OA mice chondrocytes were detected. Compared with the normal control, the expression levels of LC3 I / II and p62 in OA group were significantly increased, indicating that autophagy in OA was inhibited. MiR-145 promotes autophagy of mouse chondrocytes by down regulating FRS2, and reduces the expression levels of LC3 I / II and p62, which indicates that overexpression of miR-145 can significantly enhance the autophagy activity of articular cartilage. ［Conclusion］ miR-145 can significantly improve the viability of chondrocytes by inhibiting FRS2 to promote autophagy, and thus play a role in cartilage protection.