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目的 白细胞可以导致缺血细胞损伤，内皮细胞上表达的细胞间粘附分子－１（ＩＣＡＭ－１）有利于白细胞迁移至组织。本研究目的是对小鼠大脑中动脉栓塞（ＭＣＡＯ）后脑内ＩＣＡＭ－１ 蛋白在组织中表达和含量进行检测。方法 通过对成年雄性ＣＤ－１ 小鼠使用血管腔内尼龙线栓塞术，造成０、３、６、１２、２４、４８ 和７２ ｈ 的持续性大脑中动脉栓塞。缺血程度由激光多普勒流量仪确定，缺血脑组织ＩＣＡＭ－１ 的阳性表达由免疫组化技术检测，并用免疫沉淀和Ｗｅｓｔｅｒｎ 印迹来定量。结果 在大脑中动脉栓塞后，小鼠缺血脑半球的表面脑血流量减少到基准值的９％ ～１５％ 。各组间大脑中动脉栓塞过程中的脑血流量无显著差异。免疫组化技术显示，缺血中心区和末影区都见ＩＣＡＭ－１ 阳性的微血管内皮细胞，从缺血中心到缺血边缘区微血管内皮细胞表达ＩＣＡＭ－１ 出现增高的趋势。免疫沉淀和Ｗｅｓｔｅｒｎ 印迹分析结果表明，缺血区ＩＣＡＭ－１的表达在大脑中动脉栓塞后３ ｈ 增高，６～１２ ｈ 达到高峰，并持续到７２ ｈ。结论 研究表明，在持续性大脑中动脉栓塞的小鼠中检测到ＩＣＡＭ－１ 表达明显升高，因为在持续局灶性大脑中动脉缺血后ＩＣＡＭ－１ 可介导白细胞和内皮细胞粘附，加速
The purpose of leukocytes can cause ischemic cell damage, and the expression of intercellular adhesion molecule-1 (ICAM-1) on endothelial cells favors leukocyte migration to the tissues. The aim of this study was to detect the expression and content of ICAM-1 protein in the brain after middle cerebral artery occlusion (MCAO) in mice. Methods Continuous intracranial arterial embolization was performed on adult male CD-1 mice at 0, 3, 6, 12, 24, 48, and 72 h. The degree of ischemia was determined by laser Doppler flow cytometry. The expression of ICAM-1 in ischemic brain tissue was detected by immunohistochemistry and quantified by immunoprecipitation and Western blotting. Results After the middle cerebral artery occlusion, the cerebral blood flow in the ischemic hemisphere of mouse decreased to 9% -15% of the baseline value. There was no significant difference in cerebral blood flow during middle cerebral artery occlusion among groups. Immunohistochemistry showed that ICAM-1 positive microvascular endothelial cells were seen in the ischemic center and the terminal area, and the ICAM-1 expression increased from the ischemic center to the microvascular endothelial cells in the marginal zone of ischemia. Immunoprecipitation and Western blot analysis showed that the expression of ICAM-1 in the ischemic area increased 3 h after middle cerebral artery occlusion and peaked at 6 to 12 h and lasted for 72 h. Conclusions Studies have shown that ICAM-1 expression was significantly elevated in patients with persistent middle cerebral artery occlusion as ICAM-1 mediates leukocyte and endothelial cell adhesion after persistent focal middle cerebral artery ischemia, accelerate