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."/>
Effect of Anti ICAM-1 Antibody on HypoxicIschemic Brain Damage in Neonatal Rats
Abstract 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.
WANG Suo-Ying,SONG Shao-Ming,WU Jian-Nong et al. Effect of Anti ICAM-1 Antibody on HypoxicIschemic Brain Damage in Neonatal Rats[J]. 中国当代儿科杂志, 2003, 5(5): 425-428.
WANG Suo-Ying,SONG Shao-Ming,WU Jian-Nong et al. Effect of Anti ICAM-1 Antibody on HypoxicIschemic Brain Damage in Neonatal Rats[J]. CJCP, 2003, 5(5): 425-428.
