小鼠局灶性脑缺血模型中细胞间粘附分子-1表达升高

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

Increased Expression of Intercellular Adhesion Molecule-1 (ICAM-1) in Mouse Focal Cerebral Ischemia Model

Objective Leukocytes may contribute to ischemic cell damage.Intercellular adhesion molecule 1 (ICAM 1) expression on endothelial cells facilitats the migration of leukocytes into tissue.The aim of our study is to quantitatively measure the temporal profiles of ICAM 1 protein in mouse brain after middle cerebral artery occlusion (MCAO). Methods Adult male CD 1 mouse was received 0,3,6,12,24,48 and 72 h of permanent MCAO using an intraluminal suture technique.The degree of occlusion and extent was determined using a laser Doppler flowmetry.ICAM 1 positive expression in the ischemic regions were determined using immunohistochemistry and ICAM 1 protein was quantitatively measured using immunopreciptaion and Western blot analysis. Results After MCAO,surface cerebral blood flow (CBF) in the ischemic hemisphere was decreased to 9% 15% of the baseline in each time point of 7 8 animals.There were no significant differences in CBF measurement during occlusion.Immunohistochemistry showed that ICAM 1 positive microvascular endothelial cells were observed both in the ischemic core and perifocal region.There was a tendency for increased expression of ICAM 1 positive microvascular endothelial cells from the ischemic core to the ischemic margin.As judged by Western blot analysis,ICAM 1 expression in the ischemic hemisphere was increased at 3 h following MCAO,peaked at 6 to 12 h,and persisted 24 to 72 h. Conclusions We demonstrated that enhanced ICAM 1 expression in the permanent MCAO in mice.Because ICAM 1 mediate leukocyte endothelial adhesion and progression of leukocyte infitration after permanent focal cerebral ischemia.These studies suggested one of important roles for ICAM 1 participating in ischemic cerebral damage and pathogenesis of evolving stroke.