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目的 观察腹腔注射胰岛素或B链肽 (9～ 2 3)对NOD鼠胰岛FasL/Fas系统表达的影响。 方法 96只雌性NOD鼠随机分为B1、B2和B3三组 ,每组 32只。于 4周龄分别腹腔注射胰岛素、胰岛素B链肽和PBS ,15周龄检测胰腺Fas、FasL、CPP32蛋白 ,及IFN γ、IL 10、Fas、FasL和CPP32mRNA的表达水平。并观察 30周龄糖尿病的累积发病率。 结果 B1组和B2组较B3组糖尿病初发时间延迟 (2 2、2 4、17周 ) ,发病率下降 (37%、32 %、72 % ) ,胰岛炎积分明显减轻 (P <0 0 1) ,胰腺IFN γ、Fas、CPP32mRNA的表达 ,B1组和B2组较B3组明显减弱 (P <0 0 1) ,B1组和B2组胰腺IL 10的表达较B3组明显增强 (P <0 0 1) ,FasLmRNA的表达三组间均无统计学差异 ;胰岛细胞及炎症细胞Fas、CPP32蛋白表达 ,B1组和B2组明显弱于B3组 (P <0 0 5 )。FasL蛋白在胰岛细胞和炎症细胞的表达 3组间无统计学差异 (P >0 0 5 )。 结论 胰岛素和胰岛素B链肽免疫NOD鼠可下调Th1细胞和细胞因子效应 ,上调Th2细胞和细胞因子效应 ,进而下调胰岛 β细胞和炎症细胞FasL/Fas凋亡通路 ,延缓糖尿病发病。
Objective To observe the effect of intraperitoneal injection of insulin or B chain peptide (9 ~ 23) on the expression of FasL / Fas in pancreatic islets of NOD rats. Methods 96 female NOD mice were randomly divided into three groups of B1, B2 and B3, with 32 in each group. At 4 weeks of age, insulin, insulin B chain peptide and PBS were injected intraperitoneally. The expression of Fas, FasL, CPP32 protein and IFNγ, IL 10, Fas, FasL and CPP32 mRNA were detected at 15 weeks of age. And observed the cumulative incidence of 30 weeks of diabetes. Results The incidence of diabetes was significantly delayed in group B1 and group B2 compared with that in group B3 (22, 22, and 17 weeks), and the incidence of diabetes was significantly decreased (37%, 32% and 72%, P <0.01) ), The expressions of IFN-γ, Fas and CPP32 mRNA in pancreas were significantly decreased in group B1 and group B2 compared with group B3 (P <0.01). The expression of IL-10 in group B1 and group B2 was significantly higher than that in group B3 1). There was no significant difference in the expression of FasL mRNA between the three groups. The expressions of Fas and CPP32 in islet cells and inflammatory cells in group B1 and group B2 were weaker than those in group B3 (P <0.05). There was no significant difference in the expression of FasL protein among the three groups of islet cells and inflammatory cells (P> 0.05). Conclusion Insulin and insulin B chain peptide immunization NOD mice can down-regulate the Th1 cells and cytokines, up-regulate Th2 cells and cytokines, and then down-regulate the FasL / Fas apoptotic pathway of pancreatic β cells and inflammatory cells to delay the onset of diabetes.