糖尿病视网膜病变（DR）中小胶质细胞功能调控的机制是目前研究的热点。我们的前期研究发现缺氧、高糖环境下小胶质细胞/巨噬细胞功能异常与神经细胞凋亡和微血管屏障破坏密切相关，并证实DR环境下小胶质细胞被激活，其TXNIP和NLRP3表达均上调，而TXNIP被静默后NLRP3显著下降。基于此，本项目提出假说：高糖、缺氧环境中视网膜小胶质细胞可能通过TXNIP途径促使NLRP3炎症小体生成，从而导致视网膜神经细胞焦亡、微血管屏障破坏等一系列炎症反应进展。据此，本研究拟在野生型及TXNIP基因敲除小鼠糖尿病模型和细胞模型中探讨DR环境下视网膜中是否存在TXNIP/NLRP3轴来调控小胶质细胞功能，及其引起视网膜微血管及神经细胞发生病理改变的潜在机制，从而为把TXNIP/NLRP3轴和小胶质细胞作为研究防治DR药物的治疗靶点提供理论和实验依据。

The mechanisms of modulating retinal microglial cells in Diabetic retinopathy (DR) have received increasing concerns in current studies. Our previous studies found close association of the dysfunction of microglial/macrophages with neurocytes apoptosis and microvascular destruction, in which we derected activated microglial cells accompanied with up-regulated expression of TXNIP and NLRP3 but significant decrease of NLRP3 when TXNIP was silenced. Based on these previous findings, the current study hypothesized that hyperglycemia and hypoxia increased NLRP3 inflammasome in microglial through TXNIP pathway, which proceeds the inflammation with neurocytes pyroptosis and microvascular destruction. Actually, this study is supposed to explore the role and modulation mechanisms of TXNIP/NLRP3 axis on microglial with the application of previously established DR mice model with wild type or TXNIP knockout background and cell models mimicking diabetic retinopathy. Therefore, the current study is aimed to further clarify the potential role of microglial and TXNIP/NLRP3 axis in DR, thus providing fundamental evidence for TXNIP/NLRP3 axis and microglial as potential targets for the treatment of diabetic retinopathy.