局灶脑缺血再灌流后ICAM-1表达与白细胞浸润

The temporal profiles of ICAM-1 expression and leukocytes infiltration after focal cerebral ischemia/reperfusion

目的 探讨大鼠局灶性脑缺血再灌流后细胞间粘附分子 - 1(ICAM- 1)表达规律与白细胞浸润。方法 采用大鼠 MCA线栓闭塞 /再通法建立局灶性缺血 /再灌流模型 ,动态观察 ICAM- 1、髓过氧化物酶 (MPO)变化情况。结果 (1)鼠脑缺血 /再灌流后 MCA供血区皮质及梗死周边区的微血管 ICAM- 1表达于再灌流 6 h已增强 ,36～ 48h达高峰 ,以后逐渐减弱 ,但第 7天表达仍强于假手术组。(2 )坏死周边区神经元也表达 ICAM- 1。(3)再灌流 6 h出现白细胞浸润 ,浸润高峰在 2 4～ 36 h,6 d后恢复正常。结论 (1)缺血再灌流使微血管表达 ICAM- 1上调 ,同时也伴随坏死周边区的神经元表达 ICAM- 1。 (2 )白细胞浸润与 ICAM- 1表达规律同步。

Objective To study the temproal course of expression of ICAM-1 protein and the feature of neutrophils infiltration in rat brain after MCA occlusion/reperfusion. Methods The animal models of the MCA ischemia/reperfusion was established in Wistar rats. The expression of ICAM 1 was measured by immunohistochemistry and the neurtrophil infiltration was determined by the evaluation of MPO. Results (1)ICAM 1 immunoractivity was enhanced in microvessels in the ischemic lesion at 6h after reperfusion,reached the peak at 36～48h,and then decreased gradually,but at the 7th day,upregulation of ICAM 1 expression still existed. (2)Neurons also expressed ICAM 1 at the border of infarct. (3)MPO activity rose at 6h,reached the peak at 24～36h and then returned to near normal level at 6d. Conclusion (1)Up regulation of ICAM-1 in microvessel occured after ischemia/reperfusion,it also existed in neurons at the border of infarct. (2)The feature of neutrophils infiltration in ischemic region had the similar regularity to expression of ICAM-1.