炎症小体与糖尿病并发症

固有免疫是机体的第一道防线。其家族成员NLRP3炎症小体是炎性免疫反应的重要组成部分，它不仅是炎l生反应的“感受器”，亦是炎性反应的“调节器”。NLRP3炎症小体能够识别内源性危险信号，激活e,aspase-1，继而活化白细胞介素（IL）-1β、IL-18等细胞因子，激发炎性反应瀑布效应，在糖尿病及其并发症中起重要作用。高血糖、高血脂和高血尿酸可激活NLRP3炎症小体，活化的NLRP3炎症小体通过K＋通道模型、溶酶体破坏模型及活性氧簇模型介导糖尿病肾病、糖尿病视网膜病变和动脉粥样硬化的发生、发展。

Inflammasome and diabetic complications

The innate immune system builds up the body＇s first line.Nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 （NLRP3）,amember of theinnate immune family, is indicated as an important component of the inflammatory immune response.It is not only the ＂sensor＂, but also a ＂regulator＂ of inflammation response.NLRP3 can identify endogenous danger signals,lead to the activation of caspase-1 and lhen activate eytokines interieukin （IL）-1beta,IL-18,and trigger the inflammatory cascade reaction, playing an important role in diabetes and its complications.High glucose, fatty and uric acid in blood activate NLRP3 inflammasome.The activation of NLRP3 inflammasome mediates the occurrence and development of diabetic nephropathy, diabetic retinopathy and atheroselerosis by K＋ channel, lysosome damage and reactive oxygen species model.