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目的探讨青春双歧杆菌对1型糖尿病小鼠胰岛β细胞的保护作用。方法给予1型糖尿病小鼠口服青春双歧杆菌,观察实验组和对照组体重的变化及糖尿病发病率。ELISA法测定血清、脾细胞上清IL-4和IFN-γ浓度,电镜观察胰岛超微结构变化。结果15周龄时实验组体重(23.41±1.64)g,而对照组为(22.31±1.32)g(P<0.05);实验组发病率低于对照组(P<0.05);实验组血清、脾细胞上清IL-4浓度明显高于对照组,而IFN-γ低于对照组(P<0.05);对照组残存胰岛的β细胞数目稀少,有核膜和内浆网扩张、核糖体脱颗粒和分泌颗粒空泡样变等超微结构异常,而实验组胰岛β细胞数显著多于对照组(P<0.05),且无上述超微异常。结论青春双歧杆菌通过上调IL-4水平,降低IFN-γ水平,促使免疫平衡向Th2方向偏移,且有保护胰岛β细胞超微结构的作用,在一定程度上可预防和延缓NOD鼠糖尿病的发生。
Objective To investigate the protective effect of Bifidobacterium adolescentis on islet β cells in type 1 diabetic mice. Methods Bifidobacterium adolescentis was given orally to type 1 diabetic mice, and the changes of body weight and the incidence of diabetes in experimental group and control group were observed. The concentrations of IL-4 and IFN-γ in the supernatant of serum and splenocytes were measured by ELISA. The ultrastructural changes of islet were observed by electron microscopy. Results The body weight of the experimental group was (23.41 ± 1.64) g at 15 weeks of age, while it was (22.31 ± 1.32) g in the control group (P <0.05). The incidence of the experimental group was lower than that of the control group (P <0.05) The concentration of IL-4 in the supernatant of the cells was significantly higher than that of the control group, but the level of IFN-γ was lower than that of the control group (P <0.05). The number of remaining β cells in the islets was scarce in the control group with nuclear membrane and endoplasmic reticulum dilatation. And secretory vacuolar degeneration and other ultrastructural abnormalities, while the experimental group of pancreatic β-cell number was significantly more than the control group (P <0.05), and no such abnormalities. Conclusion Bifidobacterium adolescentis can prevent and delay the progression of NOD mouse diabetes by up-regulating the level of IL-4, decreasing the level of IFN-γ, shifting the balance of immunity towards Th2 and protecting the ultrastructure of pancreatic β cells. happened.