【摘要】 目的　观察局部亚低温对大鼠局灶脑缺血再灌注损伤的保护作用及对微管相关蛋白 2 (MAP2 )表达的影响 ,探讨亚低温对脑缺血保护作用的机制。方法　用线栓法制作大鼠大脑中动脉闭塞 (MCAO)局灶脑缺血再灌注模型 ,随机分为假手术组、常温缺血组和亚低温缺血组 ,分别于栓塞 2h、6h、1 2h均再灌注 4h后处死 ,其中亚低温组于栓塞后 30min实施病灶侧脑亚低温并持续至再灌注期。处死前进行神经功能缺陷评分 ;HE染色观察病理形态学改变 ;免疫组织化学法检测MAP2 的表达 ,并进行定性和定量分析。结果　亚低温组大鼠神经功能缺陷评分明显低于常温组 (P <0 .0 5或P <0 .0 1 ) ;亚低温组神经元损伤明显减轻 ;亚低温组半影区MAP2 表达水平较常温组显著增高 (P <0 .0 1 )。结论　局灶脑缺血后 30min应用局部亚低温并持续至再灌注期能够减轻脑组织病理形态损伤程度 ,促进脑缺血后神经功能恢复 ;这种保护作用的产生与亚低温促进梗死灶周围半影区MAP2表达增强有关更多还原

【Abstract】 Objective To observe the effect of mild hypothermia on the immunoreactivity of microtubule associated protein 2 (MAP 2) after focal cerebral ischemia/reperfusion, and to investigate the relationship between MAP 2 changes and the neuroprotection of mild hypothermia.Methods The focal cerebral ischemia/reperfusion models of rats were achieved by middle cerebral artery occlusion (MCAO). The adult rats were randomly divided into sham operation group, normothermia ischemia/reperfusion group and hypothermia ischemia/reperfusion group. The two ischemic groups were respectively further divided into 3 subgroups (subjected ischemia for 2h, 6h, 12h respectively and then all reperfused for 4h, n =7 per time point). Brain mild hypothermia was achieved 30 minutes after ischemia and maintained to reperfusion period. The neurological deficit scores were determined before killing, pathohistological changes of injured neurons were demonstrated by H E staining and microscopy, and the expression of MAP 2 was assayed by immunohistochemistry and computerized image analysis system.Results Compared with the normothermia group, mild hypothermia greatly decreased the neurological deficit scores (P<0.05 or P<0.01), obviously attenuated the pathological injury of neurons, and increased the expression of MAP 2 in penumbra significantly (P<0.01).Conclusion Mild hypothermia can greatly attenuate neuronal damage through enhancing MAP 2 expression in penumbra after focal cerebral ischemia/reperfusion.更多还原