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目的:观察热休克(heatshock,HS)和缺血预处理(ischemicpreconditioningI.P)对缺血再灌注(I/R)心肌损伤的保护作用,并同时检测HS和IP后热休克蛋白72(HSP),抗氧化酶的动态变化,探讨HSP和IP对缺血再灌注心肌保护的可能机制。方法:建立HS和IP动物模型,检测HS和IP后,模型,检测HS和IP后,0、24、48、96、192hHSP表达水平的变化及再灌注后的心肌组织SOD、CAT、MDA含量变化,最后处死动物,用TTC染色测定心肌坏死范围。结果:再灌注后24h和48h两组心肌组织MDA含量减少,SOD、CAT活性明显高于对照组。对照组、HS组及IP组oh几乎无HSP表达,其表达高峰在HS和IP后24h,48h,随后逐渐降低,于192h返回基线水平。HS和IP组心肌梗死面积较对照组显著减少(P<0.01)。结论:热休克蛋白和缺血预处理均能提高抗氧化酶活性,减轻心肌缺血再灌注损伤。
OBJECTIVE: To observe the protective effect of heat shock (HS) and ischemic preconditioning I.P on myocardial injury induced by ischemia / reperfusion (I / R) and to detect the expression of heat shock protein 72 (HSP) , The dynamic changes of antioxidant enzymes to explore the possible mechanism of HSP and IP on myocardial protection after ischemia-reperfusion. Methods: HS and IP animal models were established. After HS and IP were detected, the changes of HSP24, HSP98 and HSP98 expression levels and the contents of SOD, CAT, MDA in myocardium after reperfusion The animals were sacrificed and the extent of myocardial necrosis was determined by TTC staining. Results: The content of MDA in myocardial tissue and the activity of SOD and CAT in 24h and 48h after reperfusion were significantly higher than those in control group. The control group, HS group and IP group oh almost no HSP expression, peak expression in HS and IP after 24h, 48h, then gradually decreased at 192h return to baseline levels. The area of myocardial infarction in HS and IP group was significantly lower than that in control group (P <0.01). Conclusion: Both heat shock protein and ischemic preconditioning can increase the activity of antioxidant enzymes and alleviate myocardial ischemia-reperfusion injury.