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李丽,顾文燕.Notch1/Hes1通路活化通过抑制氧化应激改善高糖诱导的心肌细胞肥大[J].中国动脉硬化杂志,2019,(3):216~220
Notch1/Hes1通路活化通过抑制氧化应激改善高糖诱导的心肌细胞肥大
Activation of Notch1/Hes1 pathway reduces high glucose-induced cardiomyocyte hypertrophy by inhibiting oxidative stress
投稿时间:2018-08-15  修订日期:2018-09-26
DOI:
中文关键词:  Notch1/Hes1信号通路  心肌细胞肥大  氧化应激
英文关键词:Notch1/Hes1 signaling pathway  cardiomyocyte hypertrophy  oxidative stress
基金项目:
作者单位E-mail
李丽 恩施土家族苗族自治州中心医院手术室,湖北省恩施市 445000 e-mail为1634598925@qq.com,e-mail为190244682@qq.com 
顾文燕 恩施土家族苗族自治州中心医院手术室,湖北省恩施市 445000 e-mail为1634598925@qq.com,e-mail为190244682@qq.com 
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中文摘要:
      目的 研究Notch1/Hes1信号通路活化对高糖诱导的心肌细胞肥大的影响,及其对氧化应激的作用。方法 原代培养大鼠心肌细胞,采用图像分析法检测心肌细胞表面积,BCA试剂盒分析细胞总蛋白含量,采用RT-qPCR和Western blot技术检测Notch1、Hes1、超氧化物歧化酶(SOD1)及诱导型一氧化氮合酶(iNOS)蛋白表达水平,相关试剂盒检测细胞匀浆中丙二醛(MDA)及一氧化氮(NO)含量。结果 与对照组比较,高糖能明显诱导心肌细胞表面积及总蛋白含量的增加(P<0.05),心肌细胞中Notch1、Hes1蛋白表达量也明显降低(P<0.05),同时氧化应激产物MDA、NO明显升高(P<0.05),并且SOD1显著降低、iNOS显著升高(P<0.05);激活Notch1/Hes1信号通路能够显著降低高糖引起的心肌细胞肥大及氧化应激损伤(P<0.05),而Notch1干扰慢病毒可阻断Notch1对心肌细胞肥大及氧化应激的上述改善作用(P<0.05)。结论 激活Notch1可以降低高糖诱导的心肌细胞肥大,其作用机制可能与降低细胞氧化应激损伤有关。
英文摘要:
      Aim To study the effect of Notch1/Hes1 pathway activation on the cardiomyocyte hypertrophy induced by high glucose (HG), and observe its role in oxidative stress. Methods Primarily cultured rat cardiomyocytes were used in the study. The cell surface areas of the cardiomyocytes were measured by an image analysis system. The cell protein content was detected by BCA method. The expression levels of Notch1, Hes1, superoxide dismutase 1(SOD1) and induction nitric oxide synthase(iNOS) were determined by RT-qPCR and Western blot. Related kits were used to measure the content of malondialdehyde(MDA) and mtric oxide(NO) in cardiomyocytes. Results Compared with control group, the cell surface areas and total protein content of the cardiomyocytes were significantly increased (P<0.05), the expression levels of Notch1 and Hes1 were significantly decreased (P<0.05), the levels of MDA, NO and iNOS were significantly increased (P<0.05), and the expression of SOD1 was greatly decreased (P<0.05) in HG-induced cardiomyocytes. Notch1 activation suppressed HG-induced cardiomyocyte hypertrophy and the levels of oxidative stress (P<0.05). These effects of Notch1 activation were abolished by Notch1 gene interference (P<0.05). Conclusion Notch1 activation reduces HG-induced cardiomyocyte hypertrophy by decreasing oxidative stress in cardiomyocyte.
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