【摘要】 目的：探讨ＩＣＡＭ－１在糖尿病脑缺血再灌流损伤中的作用。方法：采用线栓法脑缺血再灌注模型，比较糖尿病及正常大鼠缺血再灌注后脑内ＩＣＡＭ－１的表达、炎性细胞浸润及梗塞大小。结果：糖尿病大鼠缺血再灌注组脑组织受到的缺血损害明显重于正常缺血再灌注大鼠组；糖尿病缺血大鼠脑内微血管内皮细胞ＩＣＡＭ－１的表达以及炎性细胞浸润程度明显高于正常缺血对照组（Ｐ＜０．０５）。结论：糖尿病可加重局灶性脑缺血再灌流损伤并增强炎性反应的程度。超负荷血糖条件下ＩＣＡＭ－１可能是加重糖尿病脑缺血再灌流损伤的机制之一。更多还原

【Abstract】 Aim: To study the role of intercellular adhesion molecule 1 (ICAM-1)s in focal cerebral ischemia-reperfusion injury in diabetic rats. Methods: By using intravascular thread model with one hour of occlusion and 24 hours of reperfusion. the ex- pression of ICAM-1 in cerebral microvascular endothelial cells, inflammatory cell infiltration and brain infarction size of dia- betic rats group were compared with those of normal rats group. Results: There was a larger infarct volume in diabetic rats group compared with the normal group (P<0. 05). The degree of up-regulation of ICAM-1 and infiltration of inflammatory cells in the ipsilateral hemisphere in diabetic group was more significant than that in normal control group. Conclusion:Dia- betes aggravates cerebral ischemia-reperfusion injury exacerbates inflammatory response to cerebral ischemia-reperfusion. I- CAM-1 may be an important factor among the mechanisms aggravating focal cerebral ischemia-reperfusion. injury in diabetes mellitus under the condition of chronic overloading (high concentration ) blood glucose.更多还原