瘦素（Leptin）和Vaspin同属于脂肪因子家族。它们与骨性关节炎（Osteoarthritis，OA）疾病密切相关。我们之前的研究表明leptin对关节软骨具有降解作用。最近我们发现OA患者体内vaspin水平显著下降，在软骨细胞中具有抗炎症和抗降解作用，且与NF-κB信号通路密切相关。同时我们的预实验结果显示在软骨细胞中vaspin具有对抗leptin介导的炎症降解作用，但是具体机制尚不明确。我们推测vaspin与leptin表达水平的失衡及相互拮抗在骨性关节炎中具有重要作用。本项目通过检测vaspin与leptin对软骨细胞代谢和滑膜炎症及血管增殖的影响，研究相互的拮抗作用；检测vaspin与leptin对软骨细胞和滑膜组织NF-κB信号通路调控，探讨相关机制；通过动物模型，从组织学阐明两者在关节退变中的拮抗机制。本研究将揭示脂肪因子相互拮抗在OA中的作用，为OA治疗提供新思路。

Leptin and visceral adipose tissue-derived serine protease inhibitor(Vaspin) both belonged to the adipokines family. They were closely related to the pathophysiology of osteoarthritis (OA). Our studies showed that leptin plays a catabolic role on articular cartilage. Recently, we demonstrated that the vaspin levels were markedly decreased in patients with OA, and vaspin prevented the inflammation and degradation of chondrocytes, which closely related to the NF-κB signaling pathway. Besides, our pre-experiment studies demonstrated vaspin suppress leptin-induced degradation on chondrocytes, while the current mechanism was still absent. We speculate that the antagonism and imbalance between vaspin and leptin may play an important role during the pathophysiology of OA. In the present study, we will inspect the metabolism induced by vaspin and leptin in chondrocytes and also inflammatory and angiogenesis in synovial tissues, and find out the antagonism role between vaspin and leptin. We will assess the effects of vaspin and leptin on the NF-κB signaling pathway changes and find out related mechanisms. Through the animal model with intra-articular injection, we will find out the precise antagonism role between these two adipokines. This project will explore the role of antagonism between adipokines during the pathophysiology of OA.