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晚期糖基化终产物对心肌细胞葡萄糖转运蛋白1表达的影响及机制研究 被引量:3

Effect of advanced glycation end products on GLUT1 expression in cardiomyocytes and its mechanism
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摘要 目的探讨晚期糖基化终产物(AGEs)对心肌细胞葡萄糖转运蛋白1(GLUT1)表达的影响,以及p38丝裂原活化蛋白激酶(p38MAPK)在此过程中的作用。方法采用酶消化法原代培养SD大鼠乳鼠心肌细胞,建立胰岛素抵抗模型,给予不同干预,用实时定量聚合酶链反应(real-Time PCR)和蛋白印迹方法检测m RNA及GLUT1和p38MAPK的蛋白表达水平。结果胰岛素抵抗心肌细胞有GLU1表达,其中对照组与BSA组GLU1表达比较差异无统计学意义(P>0.05),糖化白蛋白AGE-BSA可诱导其GLU1表达降低,AGE-BSA组与对照组比较差异有统计学意义(P<0.05)。但在阻断p38MAPK途径后表达量明显上升(P<0.05),对照组与BSA组比较,p38MAPK磷酸化水平差异无统计学意义(P>0.05),AGE-BSA可导致p38MAPK磷酸化的增加,AGE-BSA组与对照组比较差异有统计学意义(P<0.05)。结论糖基化终产物AGEs可诱导胰岛素抵抗心肌细胞GLUT1 mRNA和蛋白表达降低,此过程与p38-MAPK磷酸化增加有关。 Objective To investigate the effect of advanced glycosylation end products(AGEs) on the expression of glucose transporter 1(GLUT1) in cardiomyocytes through the establishment of insulin resistant model,so as to determine the effect of p38 mitogen-activated protein kinase(p38 MAPK) in this process.Methods The cardiomyocytesin neonatal SD rats were primary cultured by enzymatic digestion,and the models of insulin resistance were es-tablished and given with different interventions.The m RNA and protein expression levels of GLUT1 and p38 MAPK were determined by real-time PCR and Western blot.Results There was GLU1 expression in insulin resistant cardiomyocytes.There was no statisticallysignificant difference in the GLU1 expression between the control group and BSA group(P〈0.05).AGE-BSA could induced a decrease of GLU1 expression,and there was statistically significant difference between the AGE-BSA group and control group(P〈0.05).However,the expression significantly increased after blocking the p38 MAPK pathway(P〈0.05).There was no significant difference in the phosphorylation level of p38 MAPK between the control group and BSA group(P〉 0.05).AGE-BSA could induce the increase of p38 MAPK phosphorylation.There was statistically significant difference between the AGE-BSA group and control group(P〈0.05).Conclusion AGEs may induce the decrease of GLUT1 m RNA and protein expression in insulin resistant cardiomyocytes.This process is related to the increase of p38-MAPK phosphorylation.
作者 李瑾 白瑞 秦卫伟 梁斌 Li Jin;Bai Rui;Qin Weiwei;Liang Bin.(Department of Cardiology, the Second Hospital of Shanxi Medical University, Taiyuan 030001, China)
出处 《中国药物与临床》 CAS 2018年第4期512-514,共3页 Chinese Remedies & Clinics
基金 山西省科技攻关项目(20140313015-12)
关键词 葡萄糖转运体1型 糖基化终产物 高级 肌细胞 心脏 Glucose transporter type 1 Glycosylation end products, advanced Myocytes, cardiac
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