补体抑制剂可减少补体过度激活带来的自身免疫损伤，从而可用于治疗补体系统

Complement inhibitors can reduce autoimmune damage caused by excessive complement activation, and can be used to treat a variety of autoimmune diseases mediated by the complement system. C57 mice were injected with streptozotocin to construct a diabetes model, given CR2-Crry intervention treatment, and blood glucose, Insulin and IL-10 levels were measured. The pancreatic sections were separated by HE staining and immunohistochemistry to observe the degree of inflammation and infiltration of pancreatic islets, TUNEL method to observe the apoptosis of pancreatic β-cells, and immunohistochemistry to detect the expression of Insulin, Caspase 3 and IL-10 in the pancreas. Western Blot and RT-PCR methods were used to detect the expression of Bcl-2, Caspase 3 and PDX-1 protein and RNA in the pancreas. Proteomics detection of complement regulatory molecule CR2-Crry intervention treatment of protein changes in diabetic mice, to explore its molecular mechanism. The islet β-cells were used to construct a β-cell injury model, palmitic acid was used as an inducing factor to establish a β-cell injury model, the β-cell injury model was treated with CR2-Crry, and the protein expression changes in palmitic acid-induced β-cell injury were detected, and CR2-Crry was explored The impact on diabetes has guiding significance for targeted therapy of complement inhibitors.

Supplement inhibitors can reduce autoimmune damage caused by overactivation of supplements, which can be used to treat a variety of autoimmune diseases mediated by the complement system. C57 mice injected streptomycin to build a diabetes model, gave CR2-Crry intervention therapy, and took serum to measure blood sugar, Insulin, and IL-10 levels. Separation pancreatic slice HE staining and immunogroupization observed the degree of inflammation immersion of islets, TUNEL method observed islet β apoptosis and immunogroup detection of pancreatic Insulin, Caspase 3 and IL-10 expressions. The Western Blot and RT-PCR methods detect expression of Bcl-2, Caspase 3, and PDX-1 proteins and RNA in the pancreas. Proteomics detects protein changes in the complementary regulatory molecule CR2-Crry intervention in the treatment of diabetic mice and explores their molecular mechanisms. Using islet β cells to build β cell damage model, palmic acid as an inducing factor to establish islet β cell damage model, CR2-Crry treatment β cell damage model, detection of palmic acid induced β cell damage protein expression changes, to explore the impact of CR2-Crry on diabetes, the targeted treatment of supplement inhibitors has guiding significance.

Complement inhibitors can reduce the autoimmune damage caused by over activation of complement, which can be used to treat a variety of autoimmune diseases mediated by complement system. C57 mice were injected with streptozotocin to establish diabetes mellitus model, and given CR2 crry intervention treatment. Serum glucose, insulin and IL-10 levels were measured. He staining and immunohistochemistry were used to observe the degree of inflammatory infiltration of pancreatic islets, TUNEL method was used to observe the apoptosis of pancreatic β cells, and immunohistochemistry was used to detect the expression of insulin, caspase 3 and IL-10. Western blot and RT-PCR were used to detect the expression of Bcl-2, caspase 3 and PDX-1 protein and RNA in pancreas. Proteomics was used to detect the protein changes of CR2 crry in diabetic mice and to explore its molecular mechanism. The model of pancreatic β - cell injury was established by using pancreatic β - cells and palmitic acid as the inducing factor. The model of pancreatic β - cell injury was treated with CR2 crry. The changes of protein expression in palmitic acid-induced β - cell injury were detected, and the effect of CR2 crry on diabetes mellitus was discussed, which has guiding significance for targeted therapy of complement inhibitors.<br>