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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 study the pathological relationship between adhesion molecules and leucocytes and cerebral ischemia / reperfusion injury, the expression of intercellular adhesion molecule-1 (ICAM-1) in cerebral ischemic area of 36 Sprague-Dawley rats was detected by in situ hybridization and immunohistochemistry Cell-associated antigen (LFA-1) -positive cell infiltration was observed. The results showed that the expression of ICAM-1mRNA in capillary endothelial cells in cerebral ischemic area occurred in 1h after cerebral ischemia and peaked at 1h after cerebral ischemia / 8h after reperfusion. However, the expression of ICAM-1 protein in capillary ischemic area occurred at 1h after cerebral ischemia / 2h after reperfusion and peaked at 1h after cerebral ischemia / 16h after reperfusion. The aggregation of L FA-1 positive cells in cerebral ischemic area occurred in cerebral ischemia for 1 hour, and the number of L FA-1 positive cells increased gradually with the reperfusion time prolonged. The results suggest that cerebral ischemia / reperfusion can induce the expression of ICAM-1m RNA and protein in the ischemic vascular endothelial cells, which in turn leads to the infiltration of leukocytes in the ischemic area, which may be the pathological mechanism of cerebral ischemia / reperfusion injury one.