目的： 研究脑缺血区血管细胞粘附分子-1（VCAM-1）表达和单核/巨噬细胞浸润与脑缺血的病理联系。方法： 运用免疫组化染色方法和局部脑缺血/再灌流模型探查40只SD大鼠脑缺血区VCAM-1阳性血管和单核/巨噬细胞的数量变化及其变化发生的时程。结果： 大鼠脑缺血区微血管内皮细胞VCAM-1表达发生在脑缺血1 h，并在16 h的再灌流期间，其表达逐渐增加，显示明显的时间依赖性变化。单核/巨噬细胞在脑缺血区的浸润发生在脑缺血1 h/再灌流2 h，并随再灌流时间的延长，其数量逐渐增加，在再灌流16 h，其数量最多，其浸润也显示明显的时间依赖性变化。脑缺血区血管内皮细胞VCAM-1表达的时相与单核/巨噬细胞浸润的时相基本一致。结论： 脑缺血诱导缺血性血管内皮细胞表达VCAM-1和诱导单核/巨噬细胞在脑缺血区浸润。此结果提示VCAM-1和单核/巨噬细胞可能参与缺血性脑损伤的病理过程。%AIM： To study the pathological relationship of vascular cell adhesion molecule-1 (VCAM-1) expression and monocyte/macrophage infiltration with focal brain ischemia. METHODS: Immunohistochemical technique and focal brain ischemia/reperfusion model were used in the study in order to explore profiles and time-course of VCAM-1 expression and monocyte macrophage (ED2 positive cell) infiltration in ischemic rat brain. RESULTS: VCAM-1 was up-regulated in microvascular endothelial cells in ischemic cortex at 1h postischemia, and continuously expressed during the time of reperfusion. ED2 positive cells infiltrated into ischemic cortex at 1h iscehmia/ 2h reperfusion and then ED2 positive cells increased gradually with the time of reperfusion, ED2 positive cell infiltration showed apparently relationship with VCAM-1 expression, and both of them exhibited the some changes of time-dependence. CONCLUSION: Cerebral ischemia induced VCAM-1 expression and ED2 positive cell infiltration and VCAM-1 may regulate the recruitment of ED2 positive cells in the ischemic brain region. The results suggested that VCAM-1 and ED2 positive cells may be participated in the pathogenesis of cerebral ischemic injury.
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