大鼠脑缺血区细胞间粘附分子ICAM-1表达和LFA-1阳性细胞浸润的研究

研究粘附分子和白细胞与脑缺血／再灌流损伤的病理联系，运用原位杂交和免疫组化技术对36只SD大鼠脑缺血区细胞间粘附分子（ICAM－1）表达和淋巴细胞机能相关抗原（LFA－1）阳性细胞浸润进行了观察。结果显示，脑缺血区的毛细胞血管内皮细胞表达ICAM－1 mRNA发生于脑缺血1h，在脑缺血1h／再灌流8h达到高峰。而脑缺血区毛细血管ICAM－1蛋白质的表达则发生于脑缺血1h／再灌流2h，高峰出现于脑缺血1h／再灌流16h，LFA－1阳性细胞在脑缺血区的聚集发生在脑缺血1h，并随再灌流时间延长，其聚集数量逐渐增加。结果提示，脑缺血／再灌流能诱导缺血区的血管内皮细胞表达ICAM－1 mRNA和蛋白质，进而导致白细胞在脑缺血区的浸润，此可能是脑缺血／再灌流损伤的病理机制之一。

A STUDY OF ICAM-1 EXPRESSION AND LFA-1 POSITIVE CELL INFILTRATION IN ISCHEMIC BRAIN ISCHEMIA IN RATS

To reveal the time course and the cell types of ICAM 1 mRNA and protein expression, and the time course of LFA 1 positive cell infiltration and the relationship with ICAM 1 expression, we explored profiles of ICAM 1 expression and LFA 1 positive cell infiltration in the ischemic brain by using immunohistochemical ABC and in situ hybridization techiques. The results showed that ICAM 1 mRNA expression was detected at capillary endothelial cells in ischemic cerebral cortex at 1h ischemia and peaked at 1h ischemia/8h reperfusion. ICAM 1 protein expression was detected at capillary walls in postischemia cerebral cortex at 1h ischemia/2h reperfusion and peaked at 1h ischemia/16h reperfusion. LFA 1 positive cells infiltrated into ischemic cerebral regions at 1h ischemia and increased continually during 16h reperfusion. The results suggested that ICAM 1 regulated leukocytic infiltration in ischemic brain and participated in ischemic cerebral injury.