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去甲肾上腺素诱导热休克蛋白70保护心肌细胞的机制
Expression of heat shock protein 70 induced by norepinephrine preconditioning on cardiomyocytes
【摘要】 目的探讨去甲肾上腺素预处理心肌细胞后诱导心肌热休克蛋白70(HSP70)的表达及其对心肌细胞保护作用机制。方法 Wistar大鼠乳鼠心肌细胞培养,分为3组:对照组:心肌培养3~5天未施加任何因素;缺氧/复氧组:心肌细胞培养3~5天后,模拟缺氧(加入饱和氮气pH 6.8 D-Hank’s液培养细胞)3 h,复氧(用含20%新生牛血清的DMEM液培养细胞)孵育6 h;去甲肾+缺氧/复氧组:模拟缺氧前30 min加入100 nmol/L去甲肾,其它同缺氧/复氧组。测定心肌HSP70和bcl-2以及相关的细胞凋亡指标。结果 HSP70和bcl-2的表达在去甲肾+缺氧/复氧组明显高于缺氧/复氧组,去甲肾+缺氧/复氧组的细胞凋亡率明显低于缺氧/复氧组。结论去甲肾上腺素预处理可能通过诱导心肌组织HSP70和bcl-2高表达,发挥其对供心的保护作用。
【Abstract】 Objective To investigate the expression of heat shock protein 70(HSP70) induced by norepinephrine preconditioning on cardiomyocytes.Methods The neonatal rat cardiomyocytes were cultured.The cardiomyocytes were divided into 3 groups.Control group: The cells were cultured for 72 h,without any treatment.Hypoxia/Reoxygenation group(H/Re): The cells were cultured for 3 h.In hypoxia incubator(which contained 95%N 2.5%CO2) and reoxygenation for 6 h.Norepinephrine+Hypoxia/reoxygenation group(NE+H/Re): Prior to hypoxia,the cells were treated by 100 nmol/L NE.The other procedures were the same Hypoxia/reoxygenation group.The expressions of HSP70 and bcl-2 were detected and the apoptotic rate was tested.Results The expressions of HSP70 and bcl-2 were increased in NE+ Hypoxia/reoxygenation group compared with that in Hypoxia/Reoxygenation group.The apoptotic rate of NE+ Hypoxia/reoxygenation group was lower than that of Hypoxia/Reoxygenation group.Conclusion NE preconditioning can induce the expression of HSP70,which protects hypoxia cardiomyocytes.
【Key words】 preconditioning; heat shock protein 70; bcl-2; myocardial protection;
- 【文献出处】 哈尔滨医科大学学报 ,Journal of Harbin Medical University , 编辑部邮箱 ,2012年01期
- 【分类号】R363.2
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