摘要
目的探究miR-183-5p对2型糖尿病小鼠胰岛素抵抗的改善作用及可能机制。方法 30只SPF级C57BL/6N雄性小鼠随机分对照组(Control)、胰岛素抵抗组(IR)和agomiR组,每组10只。检测各组小鼠空腹血糖、葡萄糖耐量和胰岛素耐量;生物信息学预测miR-183-5p靶基因,并通过双荧光素酶报告基因实验验证;Real-time qPCR检测肝组织EGR1 mRNA表达;Western blot检测肝组织EGR1蛋白表达。结果过表达miR-183-5p降低胰岛素抵抗小鼠血糖,改善小鼠葡萄糖耐受能力和对胰岛素敏感性;EGR1是miR-183-5p的下游靶基因,过表达miR-183-5p降低胰岛素抵抗小鼠肝组织EGR1 mRNA和蛋白表达水平。结论 miR-183-5p增加胰岛素抵抗小鼠胰岛素敏感性,其机制可能与靶向抑制EGR1表达有关。
Objective To explore the effect of miR-183-5 p on insulin resistance in type 2 diabetic mice and its possible mechanism. Methods Thirty SPF C57 BL/6 N male mice were randomly divided into Control group, insulin resistance group and agomir group, with 10 mice in each group. Fasting blood glucose, glucose tolerance and insulin tolerance of mice in each group were detected. The target genes of miR-183-5 p were predicted by bioinformatics and verified by dual luciferase reporter gene assay. Real-time qPCR was used to detect the expression of EGR1 mRNA in liver tissues. Western blot was used to detect the expression of EGR1 in liver tissues. Results Overexpression of miR-183-5 p could decrease blood glucose and improved glucose tolerance and insulin sensitivity in insulin resistant mice. EGR1 is the downstream target gene of miR-183-5 p, and overexpression of miR-183-5 p could reduce the level of EGR1 mRNA and protein in the liver tissues of insulin resistant mice. Conclusion miR-183-5 p can increased insulin sensitivity in insulin resistant mice, and the mechanism may be related to the targeted inhibition of EGR1 expression.
作者
赵晓伟
刘宇
李铁
邸蕴华
李楠
ZHAO Xiao-wei;LIU Yu;LI Tie;DI Yun-hua;LI Nan(Department of Endocrinology,Affiliated Central Hospital of Shenyang Medical College,Shenyang 110024;Department of Endocrinology,Affiliated Hospital of Liaoning University of Traditional Chinese Medicine,Shenyang 110033,China)
出处
《解剖科学进展》
CAS
2021年第5期588-591,共4页
Progress of Anatomical Sciences
基金
辽宁省自然基金(20180551277)。
