The present study aimed to clarify the protective effect of administration of an antiintercellular adhesion molecule-1 (ICAM-1) antibody (1A29) on neurological damage after global cerebral ischemia/reperfusion in rats. Global cerebral ischemia/reperfusion was produced by four-vessel occlusion for 30 min followed by reperfusion for 24 h. Animals were randomly divided into four groups: PC group (n = 10), PI group (n = 10), PR group (n = 10), and PM group (n = 10). Rats in the PC group were administered isotype-matched control antibody at a dose of 1 mg/kg IV. Rats in the PI group, PR group, and PM group were infused with 1A29 at a dose of 1 mg/kg IV before ischemia, upon reperfusion, and 4 h into reperfusion, respectively. All animals were sacrificed after reperfusion for 24 h. Cerebral sections were stained with hematoxylin and eosin for histological evaluation. The brain wet-to-dry ratio and neurological deficits were evaluated. In comparison to the PC group, the counts of polymorphonuclear leukocytes (PMNLs) and macrophages (MPhi) decreased significantly in the PI, PR, and PM groups (P < 0.01). In comparison to the control antibody group, the brain wet-to-dry ratio and the percent infarct volume were significantly reduced in rats receiving 1A29 antibody (P < 0.05 and P < 0.01, respectively). In comparison to the PC group, with a median neurological score of 2.5, mild deficits were noted in the PI, PR, and PM groups (median neurological scores were 1.6 to 1.8) (P < 0.05). 1A29 antibody decreased the counts of PMNLs and MPhi and the neurological score and it reduced the brain wet-to-dry ratio and the infarct volume, suggesting that anti-ICAM-1 antibody provides neuroprotection after global cerebral ischemia/reperfusion injury in rats.