热处理在脑缺血再灌注损伤中的作用及其机制

摘要

Objective: To explicit effects of heat stress in process of brain ischemia reperfusion and its mechanism.Method: Rats were randomly divided into heat stress group and control group. The expression of hsp70 and activity of superoxide dismutase (SOD) and malondlaldehyde (MDA) were compared between the two groups at 12 h after ischemia reperfusion 10 min.Result: In the heat stress group, activity of SOD and expression of HSP70 were higher than those of the control group, but activity of MDA was lower than that of the control group.Conclusion:Heat stress induced HSP70 mediated protective effects of brain ischemia reperfusion injury, free radical scavenging and repair scathing proteins on the brain might cause the function.%目的：明确热处理对脑缺血再灌注损伤的作用及其机制。方法：将实验大鼠随机分为热处理组与对照组，对比观察两组动物脑缺血10 min再灌注后12 h时脑组织内HSP70的表达及超氧化物歧化酶（SOD）与丙二醛（MDA）的活力。结果：热处理组的SOD活性及HSP70蛋白的表达于缺血再灌注后明显高于对照组，而MDA的活性明显低于对照组。结论：热处理诱导产生的HSP70可能对脑缺血再灌注损伤有保护作用。热处理可能是通过HSP70清除脑组织自由基和修复脑组织损伤蛋白质，进而实现对脑缺血再灌注损伤的保护作用。