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缺氧复氧诱导大鼠心肌细胞内质网应激反应
引用本文:马青变,高炜,郭艳红,赵春玉,薛林,唐朝枢.缺氧复氧诱导大鼠心肌细胞内质网应激反应[J].北京大学学报(医学版),2005,37(4):386-388.
作者姓名:马青变  高炜  郭艳红  赵春玉  薛林  唐朝枢
作者单位:1. 北京大学第三医院心血管科,北京,100083
2. 北京大学第一医院心血管科,北京,100083
3. 北京大学医学部心血管所,北京,100083
摘    要:目的:观察大鼠心肌细胞缺氧复氧时内质网应激蛋白表达的改变及其意义,以探讨心肌缺血再灌注损伤与内质网应激的关系.方法:原代培养乳鼠心肌细胞,缺氧5.5 h后复氧2~24 h制备缺氧复氧损伤模型,用Western blot和RT-PCR方法测定内质网应激蛋白GRP78表达水平.2-脱氧葡萄糖作为本实验的阳性对照,2-脱氧葡萄糖孵育心肌细胞10 h,用Western blot和RT-PCR检测GRP78表达水平.结果:缺氧复氧处理的心肌细胞活力减低,胞内乳酸脱氢酶漏出.与对照组比较,缺氧复氧组心肌细胞内质网应激蛋白GRP78在蛋白及mRNA水平表达均于复氧后2 h开始增加,4 h达峰值,蛋白水平为对照组的142%,mRNA水平为对照组的200%,表达的增加可持续到复氧24 h.结论:缺氧复氧可以诱导心肌细胞内质网应激.

关 键 词:心肌再灌注损伤  内质网  应激  热休克蛋白质类  大鼠  缺氧  氧诱导  大鼠心肌细胞  内质网应激反应  Hypoxia  cardiomyocyte  neonatal  rat  cultured  endoplasmic  reticulum  stress  可持续  蛋白水平  峰值  表达水平  mRNA  白及  细胞内质网  比较  对照组  乳酸脱氢酶  细胞活力
文章编号:1671-167X(2005)04-0386-03
修稿时间:2004年11月29日

Hypoxia/reoxygenation induced endoplasmic reticulum stress in cultured neonatal rat cardiomyocyte
MA Qing-bian,GAO Wei,GUO Yan-hong,ZHAO Chun-yu,XUE Lin,TANG Chao-shu.Hypoxia/reoxygenation induced endoplasmic reticulum stress in cultured neonatal rat cardiomyocyte[J].Journal of Peking University:Health Sciences,2005,37(4):386-388.
Authors:MA Qing-bian  GAO Wei  GUO Yan-hong  ZHAO Chun-yu  XUE Lin  TANG Chao-shu
Institution:Department of Cardiology, Peking University Third Hospital, Beijing 100083, China.
Abstract:Objective: To investigate the effect of hypoxia/reoxygenation on endoplasmic reticulum stress in cultured neonatal rat cardiomyocytes. Methods: Neonatal rat cardiac myocytes in primary culture were exposed to hypoxia for 5.5 hours and subsequently reoxygenation for 2-24 hours. Western blot and RT- PCR were applied to monitor the expression change of GRP78(glucose regulated protein 78). 2-deoxy-D-glucose(2-DG) was the positive control of this study. Then Western blot and RT- PCR were used to examine the expression of GRP78. Results: Cell viability was decreased obviously after hypoxia/reoxygenation. Compared with untreated cells, the GRP78 content of the cells had increased significantly in the hypoxia/reoxygenation cells. The level of GRP78 protein and mRNA elevated from the points of 2 hours to 24 hours after reoxygenation, and increased most obviously at the point of 4 hours after reoxygenation.(4 hours: protein level 142% of the control, mRNA level 200%). 2-DG could induce the increasing expression of GRP78 in a concentration-dependent manner from 10-50 mmol/L. Conclusion: Hypoxia/reperfusion can induce endoplasmic reticulum stress in rat cardiomyocytes.
Keywords:Myocardial reperfusion injury  Endoplasmic reticulum  Stress  Heat-shock proteins  Rats  
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