热休克预处理对大鼠缺血再灌注心肌保护作用机制的探讨

目的:观察心肌缺血再灌注时P-选择素（Ps）表达情况；探讨热休克蛋白(HSP)对缺血再灌注心肌Ps及细胞凋亡表达的影响。 方法:成年雌性Wistar（n=40）大鼠随机分为3组。热休克组全麻后高热处理造成热休克动物模型，对照组及假手术组仅予全麻处理。24 h后热休克组及对照组结扎左冠状动脉前降支(LAD)1 h，再灌注2 h造成心肌缺血再灌注动物模型。假手术组只于LAD处穿线而不结扎。术毕测心梗范围、HSP70、Bax、Bcl-2、Ps、凋亡细胞及血清CK-MB。 结果:热休克组HSP70表达高于对照组及假手术组(P<0.05)，后两组无明显差别(P>0.05)；热休克组心梗范围小于对照组(P<0.05)，CK-MB值低于对照组(P<0.01)，凋亡细胞、Bax及Ps表达低于对照组(P<0.05)，两组Bcl-2表达无显著差别(P>0.05)；假手术组无Ps表达。 结论:HSP70可抑制缺血再灌注诱导的心肌细胞凋亡，抑制Bax表达致Bax/Bcl-2比值下降为其机制之一；Ps参与心肌缺血再灌注损伤；HSP70可能有抑制心肌Ps表达的作用，这或许是热休克预处理对大鼠缺血再灌注心肌的另一保护机制。

Protective effect of heat-shock pretreatment on rat ischemia-reperfusion myocardium

AIM: To investigate the changes of expression of P-selectin(Ps) in ischemia-reperfusion myocardium and to observe the effects of heat shock protein(HSP) on the expression of Ps and apoptosis.METHODS: Mature female Wistar rats(n=40) were divided into three groups at random.Under general anesthesia,the rats in heat-shock group were subjected to whole-body hyperthermia,and those in the other two groups were treated with anesthetic alone.Twenty-four hours later,the animals in heat-shock group and in control group were subjected to surgical operative ligation of coronary left anterior descending branch(LAD) for 1 h,then accepted reperfusion for 2 h.Those in sham operation group were also performed surgical operation without LAD ligation for 3 h.After operation,the CK-MB in blood serum,infarct size of left ventricles,HSP70,Bax,Bcl-2,Ps and apoptosis cells were measured.RESULTS: The amount of HSP70 in heat-shock group was significant higher than that in control group and in sham operation group(P<0.05).There was no difference between control group and sham operation group(P>0.05).Compared with control group,the infarct size,CK-MB,apoptosis cells,Bax and Ps in heat-shock group were significantly reduced(P<0.05).However,expression of Bcl-2 was similar(P>0.05).No expression of Ps in sham operation group was detected.CONCLUSIONS: HSP70 may reduce myocardial apoptosis during ischemia-reperfusion.One of the mechanisms is that HSP70 restraines the expression of Bax and Bax/Bcl-2.Ps plays an injurious role in ischemia-reperfusion myocardium.HSP70 is likely to restrain Ps from expression,which may be one of the mechanisms by which heat-shock pretreatment plays a protective role in ischemia-reperfusion myocardium.