前交叉韧带（anterior cruciate ligament, ACL）损伤会导致关节软骨和半月板的变性，普遍采用的ACL重建术难以完全纠正膝关节异常受力，术后仍有50%的患者进展为骨性关节炎，目前对该种进行性病变的代谢分子机制仍知之甚少。腺苷是一种重要的小分子代谢产物，不仅参与机体的能量供应，还能发挥抑制炎症和促进组织修复的功能。我们前期研究发现，ACL损伤后膝关节液中腺苷含量与关节软骨及半月板变性相对应的MRI UTE-T2*值改变存在相关性。本研究将建立兔ACL重建模型和异常受力软骨细胞模型，阐述腺苷对异常力学环境下软骨细胞生物学功能的影响及其机制，并在关节腔内定期输注腺苷，评价其改善ACL重建术后MRI UTE所检测到的关节软骨及半月板变性的效果。研究所获结果将有助于阐述ACL重建术后发生骨性关节炎的分子机制，同时促进腺苷应用于关节软骨及半月板变性的治疗。

Anterior cruciate ligament (ACL) injury leading to the degeneration of knee cartilage and meniscus. The widespread reconstruction surgery is difficult to fully correct the abnormal biomechanical condition of knee, nearly 50% of postoperative patients continue developing into osteoarthritis. however, the mechanisms of metabolic molecule underlying have remained largely unexplored. In our previous study, the concentration of adenosine in synovial fluid associates with the change in MRI UTE-T2* value of cartilage and meniscus after ACL reconstruction. To further investigate this relationship between imaging findings and adenosine, we will make rabbit ACL reconstruction models and chondrocyte model to elucidate the biological function of adenosine for chondrocytes at abnormal mechanical environment and its mechanism, and then try intra-articular infusion of adenosine regularly to evaluate the improvement in meniscus and cartilage degeneration associating imaging changes after ACL reconstruction. Our study will shed light on the molecular mechanism of cartilage and meniscus degeneration after reconstruction and expand the application of adenosine to the treatment of cartilage and meniscus.