亚低温对大鼠脑缺血再灌注损伤的保护研究

The neuro-protection effect of inferior hypothermia after global cerebral ischemia and reperfusion injury in rats

目的观察亚低温对大鼠全脑缺血再灌注后海马CAI区神经元凋亡的影响,探讨亚低温对缺血再灌注脑损伤的保护作用。方法SD大鼠30只随机分为对照组(n=10),常温缺血组(n=10),亚低温组(n=10),采用改良的Pulsinelli-Brierley4血管法建立全脑缺血再灌注动物模型,缺血30min后再灌注72h,尼氏体染色观察海马区存活锥体细胞数,TUNEL法检测缺血后海马CAI区神经元凋亡情况,电镜下观察神经细胞形态学改变。结果与对照组比较,常温缺血组的海马CAI区存活的锥体细胞数目减少(P<0.01);与常温缺血组比较,亚低温组海马CAI存活的锥体细胞数目明显增多(P<0.01)。对照组、亚低温组的海马CAI区神经元凋亡数目和凋亡指数明显低于常温缺血组。在电镜下观察亚低温能明显减轻缺血后脑组织病理形态学的损害程度。结论亚低温可以抑制脑缺血再灌注后的神经细胞凋亡,对神经细胞有保护作用。

Objective To observe the morphological effect of inferior hypothermia on neuron apoptosis in hippocampal CAI of rats after global cerebral ischemia and reperfusion injury, and investigate the neuroprotection effect of inferior hypothermia. Methods Thirty SD rats were randomly divided into 3 groups： the control group（n=10）, the ischemic group（ n =10） and the inferior hypothermicgroup （ n = 10）. Using the global cerebral ischemia and reperfusion model of rat according to the procedure modified by pulsinelli et al, four arteries in rats were prepared as follows： half an hour of occlusion and 72 hours of reperfusion, then the live neurons were observed with Nissel dyeing, the apoptotic neurons in hippocampal CAI were assessed with TUNEL dyeing, and the pathologic morphological changes of all the neurons were observed under electron microscopy. Results The hippocampus CAI neurons in the ischemic group remarkably decreased compared with the control group （P 〈 0.01）. The live neurons in hippocampus CAI of the inferior hypothermic group were more than those of the ischemic group （P 〈 0.01）. Compared with the ischemic group, the quantity and apoptotic index of apoptotic neurons in hippocampal CAI in the inferior hypothermic and control groups were remarkably decreased. Under the electron microscope, the pathological changes of postischemic brain structures were markedly reduced in the inferior hypothermia group. Conclusions Inferior hypothermia may restrain apoptosis after brain isehemia and has an obvious protection effect on neurons.