各种伤病导致关节软骨受损的发生率高，严重影响患者的活动和生活质量。常规手术疗效不佳，且自体软骨移植弊端众多，而体外软骨组织构建是解决软骨组织缺损修复最为理想的方式。前期研究发现，血清因素对软骨细胞功能和体外软骨组织构建产生不利影响可能由血清中的凝血酶（Thrombin）介导，而此效应可能通过MEK-ERK1/2通路发挥作用。故提出科学假说：自然情况下Thrombin通过软骨表面PAR1受体活化MEK-ERK1/2通路诱导软骨细胞功能退变，构建出纤维软骨样组织，抑制MEK-ERK1/2通路可构建获得正常的透明软骨组织。本研究将通过抑制MEK-ERK1/2通路的方法观察Thrombin对软骨细胞功能和体外软骨组织构建的影响，并验证该方法获得的软骨组织植入后对软骨修复作用。本课题对目前软骨修复成功率低的难题及软骨受损患者的功能恢复提供创新的干预策略和方法，有着重要的临床价值和社会意义。

All kinds of injuries lead to increased rate of articular cartilage injury, which seriously affects the quality of life of patients. Conventional surgery is not effective, and autologous chondrocyte transplantation has many disadvantages, so in vitro cartilage tissue construction is the most ideal way to repair cartilage tissue defects. Previous studies have found that the adverse effects of serum on chondrocyte function and cartilage tissue construction in vitro may be mediated by Thrombin in serum, which may play a role through MEK-ERK1/2 pathway. Therefore, we propose a scientific hypothesis: Thrombin can induce the degeneration of chondrocyte function and construct fibrocartilage tissue by activating MEK-ERK1/2 pathway via PAR1 receptor on cartilage surface, and inhibit MEK-ERK1/2 pathway to construct normal hyaline cartilage tissue. In this study, we will observe the effect of Thrombin on chondrocyte function and cartilage tissue construction in vitro by inhibiting MEK-ERK1/2 pathway, and verify the effect of cartilage tissue implantation obtained by this method on cartilage repair. This topic provides innovative intervention strategies and methods for the low success rate of cartilage repair and functional recovery of patients with cartilage damage, which has important clinical value and social significance.