目的：探讨细胞间粘附分子-1(ICAM-1)单克隆抗体对新生大鼠缺氧缺血性脑损伤(HIBD)的保护作用。方法：48只7 d龄SD大鼠随机分为缺血缺氧组(A组)、ICAM-1单抗治疗组(B组)、生理盐水组(C组)和正常对照组(D组)。其中A组观察到再给氧后2 h,24 h,48 h,72 h和168 h处死,B,C,D组观察到再给氧后48 h处死。应用免疫组织化学法和HE染色观察1CAM-1在不同时间脑组织的表达和脑组织中性粒细胞浸润情况。结果：A组再给氧2 h,脑微血管内皮细胞ICAM-1微弱表达,24 h后表达开始增加,48 h达到高峰,同时受损脑组织中性粒细胞浸润也随之增加。B组再给氧48 h后,ICAM-1表达强度及中性粒细胞浸润比同时间点缺氧缺血组明显降低。结论：HIBD时ICAM-1的表达与中性粒细胞浸润密切相关,ICAM-1单抗对新生大鼠HIBD具有一定保护作用。

OBJECTIVE: To evaluate the effect of anti-intercellular adhesion molecule-1 (ICAM-1) antibody on hypoxic-ischemic brain damage (HIBD) in neonatal rats. METHODS: Forty-eight SD neonatal rats were randomly assigned into four groups; HIBD group (Group A), anti-ICAM-1 antibody treatment HIBD group (Group B), normal saline treatment group (Group C) and normal control group (Group D). The rats in the Group A were sacrificed at 2, 24, 48, 72 and 168 hs respectively after resupply of oxygen, and the rats in the Group B and C were sacrificed at 48 h after treatment. The ICAM-1 expression of the brain was detected by immunohistochemical method at different time following the re-supply of oxygen. HE staining was used to observe neutrophil infiltration in the brain tissue and pathologic characteristics of brain cells. RESULTS: The expression of ICAM-1 was light at 2 h after the re-supply of oxygen and then increased at 24 h and reached its peak at 48 h in Group A. The neutrophil infiltration in the damage brain tissue of the Group A increased simultaneously. The expression of ICAM-1 and neutrophil infiltration in Group B significantly decreased compared with those of Group A at 48 h after the re-supply of oxygen. CONCLUSIONS: The expression of ICAM-1 may be correlated with the neutrophil infiltration in hypoxic-ischemic brain tissue. The anti-ICAM-1 antibody might have protective effects against HIBD in the neonatal rat.