低温对脑缺血再灌注期间微管相关蛋白-2免疫活性的影响

目的 观察低温对脑缺血再灌注期间海马CA1区微管相关蛋白－2免疫活性的影响。方法 沙土鼠前脑缺血再灌注模型。动物随机分为假手术组、常温再灌组和低温再灌组，后两组又各分为再灌注6h、48h、96h3个亚组，每组10只。采用免疫组织化学方法结合计算机图像分析测定微管相关蛋白－2活性，观察再灌注48h、96h海马CA1区细胞膜、核膜完整，核仁清楚的锥体神经元数目。结果 常温再灌注6h、48h、96h海马CA1区微管相关蛋白－2免疫活性分别为假手术组的81％、69％和51％（P＜0．01）。低温再灌注6h、48h、96h海马CA1区微管相关蛋白－2免疫活性分别为假手术组的93％、86％和71％，均明显高于常温再灌组（P＜0．05或P＜0．01）。再灌注96h时，常温再灌组海马CA1区细胞膜、核膜完整，核仁清楚的锥体细胞数目仅为假手术组的5％（P＜0．01），低温再灌组为假手术组的47％，明显多于常温再灌组（P＜0．01）。结论 低温减轻脑缺血后延迟性神经元死亡的作用可能与其抑制微管相关蛋白－2的活性降解有关。

Effect of hypothermia on the immunoreactivity of microtubule associated protein 2 during cerebral ischemia/reperfusion

Objective To investigate the effect of hypothermia on the immunoreactivity of microtubule associated protein 2 (MAP2) during cerebral ischemia/reperfusion. Methods The cerebral ischemia models of gerbils were achieved by occluding bilateral carotid arteries, and the insult time was 10 min. The gerbils were randomly divided into sham-operation group, normothermia reperfusion group and hypothermia reperfusion group. The normothermia and hypothermia reperfusion groups were further divided into subgroups according to the reperfusion time (6 h, 48 h and 96 h). The immunoreactivity of MAP2 was determined by using immunohistochemical staining and computer image analysis system. The survival neurons in hippocampal CA1 were counted 48 h and 96 h after reperfusion. Results The immunoreactivity of MAP2 in hippocampal CA1 6 h, 48 h and 96 h after reperfusion in normothermia reperfusion group were decreased to 81%, 69% and 51% that in sham-operation group (P<0.01). The immunoreactivities of MAP2 in hippocampal CA1 in hypothermia reperfusion group were 93%, 86% and 71% that in sham-operation group, much higher than that in normothermia reperfusion group (P<0.05 or P<0.01). The number of survival neurons in hippocampal CA1 96 h after reperfusion in normothermia reperfusion group was only 5% that in sham-operation group (P<0.01), while the number of survival neurons 96 h after reperfusion in hypothermia reperfusion group was 47%, much more than that in normothermia reperfusion group (P<0.01). Conclusion Hypothemia could attenuate neuronal damage through inhibition of MAP2 degradation during cerebral ischemia/reperfusion.