炎症反应与遗传因素已被证实在糖尿病视网膜病变（DR）中具有重要作用。NLRP3作为NOD样受体家族的重要成员，其炎症体通过介导免疫应答加强机体的炎症反应，其基因突变与代谢紊乱、慢性炎症等多种疾病密切相关。目前我们发现NLRP3在DR患者中存在异常表达，据此推测NLRP3可能通过介导炎症反应参与DR的发生。为验证该假说，本项研究将以NLRP3为切入点，以DR患者及糖尿病小鼠为研究对象，进一步明确NLRP3及其炎症体在DR中的表达与活化特点，阐明线粒体活性氧诱导其活化的机制，确定DR药物局部治疗对NLRP3炎症体的影响；同时将利用我们已建立的2型糖尿病及DR患者临床资料和血液标本库，明确NLRP3基因多态性与DR的相关性，揭示其相关多态参与DR发生的生物学功能。上述研究旨在明确NLRP3参与DR的作用机制，进而为阐明DR的病因和发病机制奠定理论基础，并将为DR的个体化防治研究提供新的切入点。

The pathogenesis of diabetic retinopathy (DR) is believed to be multifactorial, with inflammation and genetic factors playing a fundamental role. NLRP3 is one of the best-studied members of the nucleotide-binding oligomerizatin domain (NOD)-like receptor (NLR) family. The dysregulation of NLRP3 inflammasome activity has been demonstrated to lead numerous proinflammatory, non-microbial human diseases. NLRP3 gene mutation is also associated with autoinflammatory diseases, metabolic disorders, and so on. We found that the higher mRNA expression level of NLRP3 in peripheral blood mononuclear cells from patients with DR. Therefore, we speculate that NLRP3 plays an important role in DR. On that basis, in the current study, expression and activation of NLRP3 inflammasome will be observed, the mechanism of mitochondrial reactive oxygen species required for NLRP3 inflammasome activation will be clarified, and the influence of local treatment of DR drugs on NLRP3 inflammasome will be determined in patients with DR and diabetic mouse. Meanwhile, using our database and blood specimen bank about patients from type 2 diabetes and DR, which have been set up completely through epidemiological investigation about DR based on inpatients and community residents, the polymorphisms of NLRP3 gene will be examined to assess their contribution to DR, and the effects of relative polymorphisms on NLRP3 expressions will be analyzed. This study will lay the theoretical basis for etiology and pathogenesis of DR, and will provide a new molecular target for individualized prevention and treatment of DR.