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作 者:戴素俊[1] 张日华[1] 朱云霞[1] 王林涛[1]
机构地区:[1]南京医科大学生物化学与分子生物学系
出 处:《南京医科大学学报(自然科学版)》2007年第5期441-443,I0001,共4页Journal of Nanjing Medical University(Natural Sciences)
基 金:南京医科大学校基金资助项目(NY02071)
摘 要:目的:探讨斑螯素(Cantharidin,蛋白磷酸酶2A抑制剂)对胰岛β-细胞的影响及作用机制。方法:将小剂量链脲佐菌素(STZ)诱导成功的1型糖尿病小鼠20只随机分为斑螯素干预组10只和糖尿病组10只,另取10只小鼠为正常对照组,动态观察空腹血糖(FBG)的变化,实验结束时检测空腹血清胰岛素(FINS)值,同时光镜下观察胰腺的组织形态学变化。结果:斑螯素干预组较糖尿病组FBG值明显下降(P<0.05),FINS值明显高于糖尿病组(P<0.01)。病理学观察发现,斑螯素干预组的胰岛体积明显大于糖尿病组,胰岛数目也较多。结论:斑螯素可以有效地改善STZ诱导的小鼠1型糖尿病残留的胰岛的结构与功能,缓解STZ诱导的小鼠1型糖尿病。Objective:To study the effect and mechanism of cantharidin (protein phosphatase 2A inhibitor) on the protection of pancreatic β-cell's death and dysfunction. Methods:Twenty type 1 diabetic mice induced by low dose streptozotocin (STZ) were randomly assigned into cantharidin-treated group (n=10) and diabetes mellitus group (n=10). Ten healthy mice were as normal control. The level of fasting blood glucose(FBG) was continuously detected. In the end, the level of fasting serum insulin(FINS) was measured and the morphology of pancreas was observed under optical microscope with HE staining. Results:The level of FBG in cantharidin-treated group was obviously lower than diabetes mellitus group(P 〈 0.05). The level of FINS in cantharidin-treated group was significantly higher than diabetes mellitus group(P 〈 0.01 ). Compared with diabetes mellitus group,the volume and cell number of islets in cantharidin-treated group were increased significantly. Conclusion:Cantharidin could obviously protect STZ-induced diabetes on mice through improving structure and function of survival islets and enhancing the insulin secretion of pancreatic β-cells.
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