Intermittent hypoxia exposure-induced heat-shock protein 70 expression increases resistance of rat heart to ischemic injury  

间歇性低氧诱导的心肌热休克蛋白70表达增加大鼠心脏对缺血损伤的耐受(英文)

作　　者：钟宁[1] 张翼[1] 方奇志 周兆年[1] 

机构地区：[1]中国科学院上海生理研究所

出　　处：《Acta Pharmacologica Sinica》2000年第5期85-90,共6页中国药理学报（英文版）

基　　金：Project supported by National Natural Science Foundation of China (Grant № 3950052).

摘　　要：AIM: To quantify the levels of HSP70 induced by different durations of intermittent (high altitude) hypoxia and to correlate them with the degree of protection of the rat heart from ischemic injury. METHODS: Reverse tran-scriptase polymerase chain reaction (RT-PCR) was used to detect the level of HSP70 mRNA expression in rat myocardium. Ischemia/reperfusion injury was presented as severity of arrhythmias induced by occlusion and reperfusion of the left anterior descending coronary artery of rat heart. RESULTS: The level of HSP70 mRNA expression increased progressively along with the duration of intermittent hypoxia training. It was 2.6, 3.6, and 3.8 folds after 14-, 28-, and 42-d exposures compared to that of normoxia. The tolerance of rat heart to ischemia/ reperfusion injury increased with hypoxia pretreatment. Such an effect was significant after rat were exposed to a 28-d intermittent hypoxia (IH). The scores for ischemia and reperfusion inducing arrhythmia for 28- and 42-d IH were 1.2±0.5, 1.0±5 and 1.0±5, 0.9±5 (P <0.01 compared with 4.0±7, 3.3±6 in normoxia rats). The overexpression of HSP70 and the increased tolerance to subsequent acute ischemia/reperfusion injury could last for 2 wk after the rats (subjected to 28 d IH) returned to normoxia. Furthermore, there was a reverse correlation between the amount of HSP70 induced and the arrhythmia occurrence ( r = - 0.98, - 0.92 for ischemia and reperfusion induced arrhythmia, P <0.01). CON-CLUSION: These results suggest that increased resistance of rat heart to ischemia/reperfusion injury after intermittent hypoxia exposure may be related to the amount of HSP70 induced.目的:定量检测暴露于间歇性低氧不同时程后心肌热休克蛋白(HSP70)表达量并探讨HSP70与大鼠心脏对缺血再灌注损伤的耐受性之间的关系。方法:结扎冠脉左前降支造成心肌缺血及再灌注模型;并以逆转录PCR方法检测大鼠心肌HSP70 mRNA的表达量。结果:间歇性低氧暴露14,28,42天后HSP70表达量分别增加2.6,3.6,3.8倍;低氧训练28天后大鼠心脏对缺血-再灌注损伤的耐受性明显增加,缺血和再灌注心律失常诱发评分(AS)显著降低;大鼠脱离低氧环境后,上述作用能够维持2周。而且HSP70的表达量与心肌耐受性的增加存在明显相关(r=0.98,0.92;P<0.01)。结论:间歇性低氧暴露后心肌对缺血-再灌注损伤耐受性的增加与HSP70的表达量有关。

关 键 词：heat-shock proteins 70 ANOXIA reverse transcriptase polymerase chain reaction ARRHYTHMIA reperfusion injury 

分 类 号：R363[医药卫生—病理学]