热应激预处理对脑缺血再灌注损伤的保护作用及可能机制

Protective effect of heat stress precondition on brain of rats with ischemia-reperfusion injury

目的:探讨热应激预处理对缺血再灌注损伤大脑的保护作用及其可能机制。方法:将实验大鼠随机分为热应激预处理组与非预处理组,对比观察两组动物脑缺血10min再灌注12h后脑组织内热休克蛋白70(HSP70)的表达、超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量、血脑屏障通透性和病理形态学改变。结果:热应激预处理组动物缺血再灌注后,脑组织内HSP70的表达及SOD活力比非预处理组高(P<0.05),而MDA含量及血脑屏障通透性比非预处理组低(P<0.05),热应激预处理组动物的脑组织损伤程度亦较非预处理组轻。结论:热应激预处理诱导产生的HSP70可能对脑组织缺血再灌注损伤起保护作用,此作用可能与HSP70清除自由基及减少血脑屏障通透性有关。

Objective To explore the protective effect of heat stress precondition on brain with ischemiareperfusion （I/R） injury and its mechanism. Methods Rats were randomized to receive heat stress precondition （precondition group） or not （non-precondition group）. The expression of heart shock protein 70 （HSP70）, activity of superoxide dismutase （SOD）, content of malondialdehyde （MDA）, permeability of blood brain barrier, and pathomorphological changes of brain were compared between the two groups 12h after I/R injury. Results As compared to non-precondition group, expression of HSP70 and activity of SOD were higher, content of MDA and permeability of blood brain barrier were lower, and injury in brain was lower in precondition group. Conclusion HSP70 induced by heart stress precondition may protect the brain against I/R injury, which may be related to the freeradical scavenging and permeability of blood barrier decreasing effect of HSP70.