星形胶质细胞炎症激活参与中枢神经系统（CNS）疾病的发生。在这过程中，细胞周期蛋白发挥重要作用。先前研究发现SYF2可通过调节细胞周期进程，促进星形胶质细胞炎症激活，并发现MCM3可与SYF2结合。鉴于此，提出星形胶质细胞炎症激活中SYF2与MCM3形成复合物，通过调节cyclin-CDKs，促进星形胶质细胞激活。本课题拟首先构建大鼠CNS炎症模型分析SYF2和MCM3的表达及相互作用变化与星形胶质细胞活化的关系；接着在星形胶质细胞炎性激活模型中分析MCM3-SYF2复合物对cyclin D1-CDK4的调节作用；在此基础上分析MCM3-SYF2复合物对星形胶质细胞激活及神经元损伤的调节作用；最后分析干预MCM3-SYF2复合物形成对CNS炎症中星形胶质细胞激活及神经元损伤的影响。课题组的研究结果为进一步阐明CNS炎症损伤后星形胶质细胞激活调节机制及CNS疾病防治方法提供理论依据。

Astrocyte inflammatory activation was involved in many central nervous system (CNS) diseases development. In this process, the cell cycle proteins play an important role. Previous studies have found SYF2 promote activate astrocytes inflammation by regulating cell cycle progression, MCM3 could combined with SYF2. In view of this, we speculated during activation of the astrocytes, SYF2 may formed complexes with MCM3, which will adjusting the signal transduction of cyclin-CDKs and promote astrocyte activation. In this project, we intends to build a rat model of CNS inflammation relationship analysis SYF2 and MCM3 expression and interaction of changes in the activation of astrocytes inflammation. And then we will analysis the MCM3-SYF2 complex formation on the activation of cyclin D1-CDK4 signal transduction in astrocytes inflammatory activation model. Based on this, we will analysis the regulatory role the MCM3-SYF2 complex on astrocytes activation and neurons injury. Finally, we will analysis of the impact of intervention the MCM3-SYF2 complex formation of CNS inflammation in astrocytes activation and neuronal damage. The results of our researches provide a theoretical basis to further clarify the mechanism of astrocyte activation and adjust the method CNS disease prevention and treatment.