摘要
目的 探讨血管内皮细胞粘附分子（Vascular cell molecule-1,VCAM-1）在脑缺血再灌注损伤中的作用和机制。方法 制作大脑中动脉梗死模型,分别于再灌注后 6h、24h、36h、48h和 7d5个时相点用兔疫组化方法观察大鼠模型脑缺血区域VCAM-1的表达,并与永久性脑梗死、假手术组和正常大鼠组比较。结果（1）正常对照组无VCAM-1的表达,假手术组在6h、24h、36h和48h均无VCAM-1的表达;（2）永久性脑梗死组6h后,在梗死周边区大脑微血管内皮细胞上和神经元上有VCAM-1的明显表达,24h表达达高峰,36～48h开始减弱,7d后完全消失;（3）缺血再灌注组6h后,在缺血周边区大脑神经元上和微血管内皮细胞上有较弱表达,24～48h达高峰,7d后在内皮细胞上仍有VCAM-1的持续表达。结论 缺血再灌注模型脑缺血区域有VCAM-1的表达,VCAM-1可能是缺血再灌注损伤的机制之一。
Objective To study the VCAM-1 impact and mechanism in the ischemia / reperfusion models of the Wistar rats. Methods The animal models of ischemia / reperfusion and permanent occlusion were established in Wister rats. The expression of VCAM-1 measured respectively at 6h, 24h, 36h,48h and 7d after reperfusion and occlusion by immunohistochemistry. Results There was the expression of VCAM-1 in the animal models of the permanent occlusion group and ischemia / reperfusion group, but not in the normal group and filse operated group; The expression of VCAM-1 in cerebral microvessels and neurons around the ischemic lesion occured at 6h after occlusion in permanent models, reached the peak at 24h, decreased at 36~48h gradually and disappeared completely after 7d. There was weak expression at 6h after reperfusion, reached peak at 24~48h and kept expres-sion after 7d. Conclusion There is the expression of VCAM-1 in ischemia/reperfusion. VCAM-1 is possible a kind of the machanisms of ischemia/reperfusion injury.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2002年第4期199-201,共3页
Journal of Apoplexy and Nervous Diseases
