骨关节炎（Osteoarthritis，OA）是最常见的肌肉骨骼系统的退行性疾病，然而尚无有效改善病情的药物。本课题组前期研究发现，N-[2-bromo-4-(phenylsulfonyl)-3-thienyl]-2-chlorobenzamide（BNTA）通过上调SOD3，显著抑制OA进展。但是OA的发生发展是由多种不同信号通路相互作用导致的，BNTA是否为多靶点药物亟需我们深入探究。前期观察到BNTA刺激后forkhead box D1（Foxd1）的表达量显著升高；体外模型证实Foxd1在软骨发育及OA进展时表达量出现明显变化。但是Foxd1抑制OA进展的详细作用机制未见报道，因而本课题主要探讨：①Foxd1在软骨发育和OA中的作用及具体作用机制，通过体内外实验进行全面探究；②通过体内外实验明确BNTA是否通过激活Foxd1发挥生物学作用，为药物治疗OA提供新的选择。

Osteoarthritis (OA) is the most common degenerative disease of the musculoskeletal system. So far, there have been no effective drugs to attenuate OA progress. Our previous study found that N- [2-bromo-4- (phenylsulfonyl) -3-thienyl]-2-chlorobenzamide (BNTA) can significantly inhibit OA progression by up-regulating the activity of SOD3. However, OA progress is induced by the interaction of different signaling pathways and networks. Whether BNTA is a multi-target drug requires further exploration. We previously observed that the expression of forkhead box D1 (Foxd1) significantly increased after BNTA stimulation; Foxd1 expression changed markedly during chondrogenesis development and OA progression in vitro. However, the detailed mechanism of Foxd1 in OA attenuation has not been reported. Therefore, this study mainly explores: (1) the function and the specific mechanism of Foxd1 in chondrogenesis development and OA progress through comprehensive in vivo and in vitro experiments; (2) whether BNTA plays the biological role by activating Foxd1, which provides new options for drug treatment of OA.