糖尿病视网膜病变（DR）神经功能异常的机制和治疗是目前研究的热点和难点。我们的前期研究发现DR早期Müller细胞功能异常与神经细胞功能损害密切相关。本研究拟采用野生基因型和IL-17A基因敲除小鼠，模拟DR环境和缺氧环境的动物模型，应用视网膜铺片、免疫荧光、RT-PCR、Western blot、TUNEL凋亡检测法、经上丘逆行标记视网膜神经节细胞，及建立相应体外细胞模型和细胞共培养等方法，研究IL-17A在DR时对Müller细胞活化和神经保护作用调控的相关机制；在此基础上，运用ERK1/2、p38抑制剂干预其信号通路激活，进一步阐明IL-17A调控Müller细胞活化和神经保护作用发挥的可能机制，进而为把IL-17A和Müller细胞作为研究防治DR药物的治疗靶点提供理论和实验依据。

The mechanisms and treatment of neurodysfunction induced by diabetic retinopathy (DR) have received increasing concerns and are difficult problems to be resolved in current studies. From our previous studies, it was found that the dysfunction of Müller cells at the early stage of DR is closely associated with neurodegeneration. Therefore, animal with IL-17A knockout and wild type C57BL/6 gene background and cell models mimicking DR and hypoxic retinopathy pathophysiologic environment will be applied to investigate the roles of IL-17A on the activation and neuroprotective effect of Müller cells in DR, by means of retinal flatmounts, immunofluorescence staining, RT-PCR and western blot assays, TUNEL staining technique, superior colliculus retrograde labeled retinal ganglion cells and co-cluture of different cells. Furthermore, ERK1/2 and p38 signaling inhibitors will be used to further clarify the modulation mechanism of IL-17A on the activation and neuroprotection of Müller cells, thus providing fundamental evidence and theoretical basis for IL-17A and Müller cells as potential targets for the treatment of diabetic retinopathy.