hERG钾通道通过降低氧化应激改善肝细胞糖代谢

发布时间：2018-07-06 17:03

本文选题：人ether-α-go-go相关基因 + 胰岛素抵抗　；参考：《首都医科大学学报》2017年02期

【摘要】：目的研究hERG钾通道(human ether-α-go-go related gene channels)在肝细胞中与糖代谢的关系。方法用hERG钾通道过表达载体转染人类肝癌细胞系(liver hepatocellular carcinoma,HepG2)细胞,通过荧光定量PCR(real-time PCR,RTPCR)和蛋白印迹(Western blotting)法检测糖代谢、糖异生、氧化应激及还原型烟酰胺腺嘌呤二核苷酸磷酸(nicotinamide adenine dinucleotide 2'-phosphate,NADPH)相关亚基的表达。结果 hERG钾通道蛋白可在肝脏细胞中表达,将hERG钾通道过表达于HepG2细胞后,糖异生相关基因葡萄糖-6-磷酸激酶(glucose-6-phosphatase,G6Pase)表达显著降低,而磷酸烯醇式丙酮酸羧激酶(phosphoenolpyruvate carboxykinase,PEPCK)表达有降低。胰岛素表达相关基因葡萄糖转运蛋白2(glucose transporter type 2,GLUT2)、胰岛素受体底物2(insulin receptor substrate,IRS-2)和腺苷酸活化蛋白激酶α亚基2[(adenosine 5’-monophosphate(AMP)-activated protein kinase),AMPKα2]的表达水平均显著增高。NADPH4种亚基p22、p47、p67和p91表达均显著降低。结论 hERG钾通道可以通过降低氧化应激改善肝细胞内糖代谢。
[Abstract]:Objective to study the relationship between human ether- 伪 -go-go related gene channels) and glucose metabolism in hepatocytes. Methods Human hepatocellular carcinoma cell line (liver hepatocellular carcinoma-HepG2 was transfected with hERG potassium channel overexpression vector. Glucose metabolism and glycosylation were detected by real-time PCR and Western blotting. Oxidative stress and the expression of reduced nicotinamide adenine dinucleotide phosphoric acid (nicotinamide adenine dinucleotide _ 2) -phosphate (nicotinamide adenine dinucleotide) -associated subunits. Results hERG potassium channel protein could be expressed in liver cells. After overexpression of hERG potassium channel in HepG2 cells, the expression of glucose-6-phosphatase G6Pase and phosphoenolpyruvate carboxykinasePEPCK decreased significantly. The expression levels of glucose transporter 2 (glucose transporter type 2 (GLUT2), insulin receptor subunit 2 (insulin receptor substrateIRS-2 and adenosine 5'-monophosphate (AMP) -activated protein kinase) protein kinase 伪 2 [(AMP) -activated protein kinase) AMPK 伪 2] were significantly increased. The expression of four subunits p22p47 p67 and p91 were significantly decreased. Conclusion hERG potassium channel can improve glucose metabolism in hepatocytes by reducing oxidative stress.
【作者单位】：首都医科大学附属北京同仁医院内分泌科;糖尿病防治研究北京市重点实验室;
【基金】：国家自然科学基金(81370946,81400824,81300726) 北京市自然科学基金(7131005) 首都医科大学附属北京同仁医院科研基金(TRYY-KYJJ-2016-013)~~
【分类号】：R587.1

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