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目的:探讨缺血后处理、缺血预处理及两者联合应用对急性全脑缺血再灌注损伤大鼠脑组织超微结构及热休克蛋白70(HSP70)的影响及其可能的机制。方法:采用改良的四血管法制造大鼠全脑缺血模型,实验分5组,假手术A组、缺血再灌注B组、缺血预处理C组、缺血后处理D组,联合处理E组,各组动物分别于再灌注结束后(6,8,24h)断头处死。采用免疫组织化学染色的方法测定大鼠脑组织中HSP70灰度值;电镜观察脑组织超微结构的变化。结果:缺血再灌注损伤后,各组脑组织HSP70表达增强,在各时间点E组HSP70表达明显高于B组、C组、D组,差异有显著性(P<0.01),C组与D组在各时间点无明显差异(P>0.05);电镜下观察B组脑组织损伤最重。E组脑组织损伤最轻,C组和D组优于B组。结论:短暂脑缺血再灌注损伤可诱导HSP70表达,有利于脑缺血再灌注后损伤神经元的修复。
AIM: To investigate the effects of ischemic postconditioning, ischemic preconditioning and their combination on the ultrastructure and heat shock protein 70 (HSP70) in brain of rats with acute global cerebral ischemia-reperfusion injury and its possible mechanism. Methods: The rat model of global cerebral ischemia was established by a modified four-vessel method. The rats were divided into 5 groups: sham operation group A, ischemia-reperfusion group B, ischemic preconditioning group C and ischemic postconditioning group D Group E, each group of animals were decapitated after reperfusion (6,8,24h). Immunohistochemical staining method was used to determine the gray value of HSP70 in rat brain. The ultrastructure of brain tissue was observed by electron microscope. Results: After ischemia-reperfusion injury, the expression of HSP70 increased in all groups. The expression of HSP70 in group E at each time point was significantly higher than that in group B, C and D (P <0.01) There was no significant difference in group D at each time point (P> 0.05). Under electron microscope, the brain tissue injury in group B was the heaviest. Brain tissue injury was the lightest in group E, group B was better than group C in group C and group D. Conclusion: The transient cerebral ischemia-reperfusion injury can induce the expression of HSP70, which is beneficial to the repair of injured neurons after cerebral ischemia reperfusion.