大鼠脑缺血区局部炎症反应的实验探查

An experimental exploration of focal inflammatory response in cerebral ischemic foci in the rat

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 1h ,并在 16h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 1h/再灌流 2h ,并随再灌流时间的延长 ,其数量逐渐增加 ,在再灌流 16h ,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

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.