小胶质细胞异常活化在RGCs凋亡中发挥着重要作用。文献报道，PPAR-γ可通过CD200R1抑制小胶质细胞活化，而CD200-CD200R1信号轴对该效应可能发挥着“开关”作用。课题组前期研究证实了PPAR-γ经CD200R1参与了视网膜小胶质细胞活化，但其在RGCs凋亡中的作用尚不清楚。基于此，我们提出假说：PPAR-γ经CD200-CD200R1轴调控小胶质细胞活化，进而抑制RGCs凋亡。课题组拟首先明确PPAR-γ经CD200R1在视网膜小胶质细胞活化中的作用；在此基础上，通过小胶质细胞和RGCs混合培养，明确CD200-CD200R1轴在上述效应和RGCs凋亡过程中扮演的角色；最终在整体水平中，靶向干预PPAR-γ和CD200-CD200R1轴，分析其对视网膜小胶质细胞活化、RGCs凋亡和视功能的影响。课题的研究结果可为视网膜退行性疾病的防治提供新的理论基础和分子靶点。

The abnormal activation of microglia plays an important role in retinal ganglion cells (RGCs) apoptosis. Previous studies reported that PPAR-γ via CD200R1 suppressed microglia activation, and CD200-CD200R1 interaction played the role of the switch in this process. We have found that PPAR-γ participated in retinal microglia activation via CD200R1. However, the role of PPAR-γ and CD200-CD200R1 signaling in RGCs apoptosis is still unclear. Therefore, we speculated that PPAR-γ via CD200-CD200R1 signaling regulates microglial activation responses in inhibition of RGCs apoptosis. We aim to determine the involvement of PPAR-γ and CD200R1 in retinal microglia activation; investigate the effect of the interaction of CD200-CD200R1 in retinal microglia activation and RGCs apoptosis in microglia-RGCs co-culture; evaluate the effect of PPAR-γ and CD200-CD200R1 intervention on retinal microglia activation, RGCs apoptosis and visual function. These results will provide new theoretical basis and molecularly targeted therapy for the treatment of retinal degenerative diseases.