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

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

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 (L FA- 1)阳性细胞浸润进行了观察。结果显示 ,脑缺血区的毛细血管内皮细胞表达 ICAM- 1m RNA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 2 h,高峰出现于脑缺血 1h/再灌流 16 h。 L FA- 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-1m RNA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。

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.\;