Zhang R L, Chopp M, Zaloga C, Zhang Z G, Jiang N, Gautam S C, Tang W X, Tsang W, Anderson D C, Manning A M
Department of Neurology, Henry Ford Hospital, Detroit, MI 48202, USA.
Brain Res. 1995 Jun 5;682(1-2):182-8. doi: 10.1016/0006-8993(95)00346-r.
Leukocytes may contribute to ischemic cell damage. ICAM-1 expression on endothelial cells facilitates the migration of leukocytes into tissue. Therefore, we measured the temporal profiles of ICAM-1 mRNA and protein in rat brain after transient (1 or 2 h) of middle cerebral artery (MCA) occlusion. Male Wistar rats (n = 86) were subjected to 1 or 2 h MCA of occlusion, or 2 h of MCA occlusion followed by reperfusion for a variety of durations ranging from 1 h to 1 week. 10 additional control animals were employed. ICAM-1 mRNA and protein were measured during ischemia and reperfusion, and immunohistochemical methods were used to identify specific cell types expressing ICAM-1. ICAM-1 mRNA was detected 1 h after the onset of ischemia. mRNA maximized at 10 h of reperfusion and persisted out to 1 week of reperfusion. ICAM-1 significantly increased in microvascular endothelial cells at 2 h of reperfusion, maximized at 46 h and persisted out to 1 week of reperfusion (P < 0.05). ICAM-1 mRNA and protein are present in ischemic brain early after the onset of ischemia and reperfusion, respectively. These data provide support for the role of ICAM-1 in mediating leukocyte-endothelial adhesion after transient MCA occlusion in the rat.
白细胞可能导致缺血性细胞损伤。内皮细胞上的细胞间黏附分子-1（ICAM-1）表达促进白细胞迁移到组织中。因此，我们测量了大鼠大脑中动脉（MCA）短暂闭塞（1或2小时）后ICAM-1 mRNA和蛋白的时间变化情况。雄性Wistar大鼠（n = 86）接受1或2小时的MCA闭塞，或2小时的MCA闭塞后再灌注不同时长（从1小时到1周）。另外使用了10只对照动物。在缺血和再灌注期间测量ICAM-1 mRNA和蛋白，并采用免疫组化方法鉴定表达ICAM-1的特定细胞类型。缺血开始后1小时检测到ICAM-1 mRNA。mRNA在再灌注10小时时达到最大值，并持续到再灌注1周。再灌注2小时时，微血管内皮细胞中的ICAM-1显著增加，在46小时时达到最大值，并持续到再灌注1周（P < 0.05）。ICAM-1 mRNA和蛋白分别在缺血和再灌注开始后早期出现在缺血性脑内。这些数据支持了ICAM-1在介导大鼠短暂MCA闭塞后白细胞-内皮细胞黏附中的作用。
