[1]黄红梅,杨茂君,羊暑艳,等.miR-17对高糖诱导的肾小管上皮细胞损伤作用的机制研究[J].国际内分泌代谢杂志,2021,41(06):623-627.[doi:10.3760/cma.j.cn121383-20200918-09037]
　Huang Hongmei,Yang Maojun,Yang Shuyan,et al.Effect of miR-17 on hyperglycemic-induced renal tubular epithelial cell injury[J].International Journal of Endocrinology and Metabolism,2021,41(06):623-627.[doi:10.3760/cma.j.cn121383-20200918-09037]
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miR-17对高糖诱导的肾小管上皮细胞损伤作用的机制研究()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
41
期数:
2021年06期
页码:
623-627
栏目:
论著
出版日期:
2021-12-20

文章信息/Info

Title:
Effect of miR-17 on hyperglycemic-induced renal tubular epithelial cell injury
作者:
黄红梅1; 杨茂君1; 羊暑艳1; 汤筱池1; 徐勇2
1成都市双流区第一人民医院内分泌科 610200; 2西南医科大学附属医院内分泌科,泸州 646099
Author(s):
Huang Hongmei1;  Yang Maojun1;  Yang Shuyan1;  Tang Xiaochi1;  Xu Yong2.
1Department of Endocrinology, Chengdu Shuangliu District First People's Hospital, Chengdu 610200, China; 2Department of Endocrinology, Affiliated Hospital of Southwest Medical University, Luzhou 646099, China
关键词:
糖尿病肾病;  miR-17;  靶向关系;  核转录因子
Keywords:
Diabetic nephropathy;  miR-17;  Targeted relationship;  Nrf-2
DOI:
10.3760/cma.j.cn121383-20200918-09037
摘要:
目的 探索miR-17在糖尿病肾病体外细胞模型中的调节作用机制。方法 选取人肾小管上皮细胞(HK-2细胞)作为模型细胞,构建高糖诱导的糖尿病肾脏体外细胞损伤模型。将细胞分为空白组(正常培养基)、葡萄糖组(高糖诱导),在高糖诱导模型组的基础上又分为miR-17 inhibitor组和NC inhibitor组。实时荧光定量聚合酶链反应(Real-time PCR)检测空白组和高糖模型组miR-17及核转录因子(Nrf-2)表达情况。再通过细胞活力检测试剂盒(CCK8)检测各组细胞增殖差异,以及流式细胞仪检测各组细胞凋亡情况。WB检测Nrf-2/血红素氧化酶-1(HO-1)信号通路相关蛋白表达,双荧光素酶报告基因检测法检测miR-17对Nrf-2的靶向关系。结果 miR-17 inhibitor能够显著促进高糖诱导的HK-2细胞增殖,且明显抑制高糖诱导的HK-2细胞的凋亡,同时miR-17能够抑制Nrf-2/HO-1信号通路,并且双荧光素酶报告基因结果显示miR-17具有靶向抑制Nrf-2的作用。结论 MiR-17能够靶向Nrf-2对高糖诱导的HK-2细胞氧化应激损伤具有一定的修复能力。
Abstract:
Objective To explore the regulatory mechanism of miR-17 in the diabetic nephropathy by in vitro model.Methods HK-2 cells were damaged by high glucose to set the model of DN in vitro. Cells were divided into blank group(normal medium), glucose group(high sugar induction), miR-17 inhibitor group and NC inhibitor group. The expression of miR-17 and Nrf-2 in the blank group and the high-glucose model group were detected by Real-time PCR. The difference of cell proliferation and apoptosis in each group were detected by CCK8 and flow cytometry. Western blot was used to detect the protein expression related to Nrf-2/HO-1 signaling pathway, and Luciferase reporter assay was used to detect the effect of miR-17 on Nrf-2.Results miR-17 inhibitor promoted the proliferation of HK-2 cells and significantly inhibited the apoptosis of HK-2 cells(renal tubular epithelial cells)which induced by high glucose. Meanwhile, miR-17 inhibited the signaling pathway of Nrf-2/HO-1, and the Luciferase reporter results showed that miR-17 had the effect of targeted inhibition of Nrf-2.Conclusion miR-17 can target Nrf-2 and repair the oxidative stress injury of HK-2 cells induced by high glucose.

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备注/Memo

备注/Memo:
基金项目:四川省科学技术厅(2019YFS0537)
通信作者:徐勇,Email:zzh1911@sina.com
更新日期/Last Update: 2021-12-10