作　　者： (杨楠）; (李雅婷）; (常晓嫒）; (朱云霞）; (董文玉）; (韩晓）;

机构地区： 南京医科大学江苏省人类功能基因组学重点实验室,南京市211166

出　　处： 《医学分子生物学杂志》 2017年第4期217-221,共5页

摘　　要： 目的 研究miR-375是否能够参与高糖引起的胰岛β细胞功能损伤,并对其具体机制进行初步探索.方法 用高糖刺激大鼠胰岛β细胞系INS-1细胞,钾刺激的胰岛素分泌（KSIS）实验检测INS-1细胞胰岛素分泌功能,运用酸乙醇抽提检测胰岛素含量,定量RT-PCR检测miR-375的表达情况.Western印记检测Neurod1的蛋白水平.结果 高糖刺激能够损伤INS-1细胞KSIS功能,降低胰岛素含量;高糖刺激同时可以升高miR-375表达水平,而过表达miR-375确实能够损伤INS-1细胞功能;miR-375能够抑制Neurod1的表达水平,干扰miR-375可以通过恢复Neurod1的表达,进而逆转高糖刺激引起的INS-1细胞KSIS功能损伤.结论 miR-375通过降低Neurod1蛋白水平介导高糖引起的胰岛β细胞功能损伤. Objective To explore the involvement of miR-375 in high glucose-induced β-cell dysfunction and the possible mechanism.Methods INS-1 cells were cultured with high glucose.Insulin secretion was detected by KCl-stimulated insulin secretion （KSIS） assay,insulin content by acid-ethanol extraction assay,miR-375 expression level by RT-PCR,and protein level of Neurod1 by Western blotting.Results High glucose induced β-cell dysfunction,and decreased insulin content.miR-375 expression was increased after exposure to glucotoxic conditions.Overexpression of miR-375 also induced β-cell dysfunction and it could directly suppress the expression of Neurod1 protein.After restoration of Neurod1 expression by knocking down miR-375,glucose-induced β-cell dysfunction was partially recovered.Conclusion Downregulation of Neurod1 expression by miR-375 mediates glucose-induced β-cell dysfunction.

关 键 词： 胰岛 细胞 功能损伤