腱骨愈合不良是韧带重建失败的重要原因，恢复腱骨界面的正常生理结构是目前运动医学研究的热点。既往研究发现巨噬细胞在腱骨愈合界面簇集并极化，但其具体作用与机制尚不清楚。课题组前期研究发现腱骨愈合界面M2型巨噬细胞极化增强，mRNA表达谱测序发现M2型巨噬细胞高表达SLPI（丝氨酸蛋白酶抑制剂），体外过表达SLPI能促进骨髓间充质干细胞成骨分化和迁移能力，提示M2型巨噬细胞可能通过分泌SLPI促进腱骨愈合。本项目拟通过极化型巨噬细胞转基因小鼠前交叉韧带重建模型，结合巨噬细胞与骨髓间充质干细胞共培养模型，明确巨噬细胞M1型或M2型极化在腱骨愈合中的作用，并在前交叉韧带重建动物模型中过表达或抑制SLPI，探讨巨噬细胞不同亚型在腱骨愈合发挥作用的细胞与分子机制，为腱骨愈合机制提供新观点，为促进腱骨愈合提供新的潜在靶点。

Poor healing of the tendon-bone is the root cause of ligament reconstruction failure. Restoring the normal physiological structure of the tendon-bone interface is currently a hot spot in sports medicine research. Macrophages accumulated and polarized at the healing interface of the tendon-bone interface, but its specific role and mechanism are still unclear. In our previous study, M2 macrophage polarization was enhanced in the tendon-bone interface. mRNA expression profile sequencing revealed that M2 macrophage highly expressed SLPI. Furthermore, overexpression of SLPI in vitro promoted osteogenic differentiation and migration of bone marrow mesenchymal stem cells (BMSC). It is suggested that M2 macrophages may promote tendon-bone healing by secreting SLPI. This project aims to establish a model of anterior cruciate ligament reconstruction in macrophage polarized transgenic mice, combined with macrophage and BMSC co-culture model to determine the role of M1 or M2 polarized macrophage in the tendon-bone healing. Through over-expressed or inhibited SLPI in the anterior cruciate ligament reconstruction model, exploring the cellular and molecular mechanisms of macrophage polarization in the pathogenesis of tendon-bone healing, providing a new perspective for the healing mechanism of tendon-bone healing and providing a new potential target for promoting tendon-bone healing.