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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

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

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【作者】 杨龙杨天和吴立荣刘君实杨永曜

【Author】 YANG Long,YANG Tian-he,WU Li-rong,LIU Jun-shi,YANG Yong-yao(Institute of Cardiovascular Diseases in Guizhou Province,Guiyang 550002,China)

【机构】 贵州省心血管病研究所贵阳医学院第一附属医院心内科贵州省心血管病研究所 贵州贵阳550002贵州贵阳550002

【摘要】 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W istar(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、Bc l-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Bc l-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/Bc l-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。

【Abstract】 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.

  • 【文献出处】 中国病理生理杂志 ,Chinese Journal of Pathophysiology , 编辑部邮箱 ,2006年11期
  • 【分类号】R363
  • 【被引频次】1
  • 【下载频次】129
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