Time course changes of ICAM-1 expression and its effective factors following brain trauma in rats

Objective To explore the possible relationship between secondary damage and expression of ICAM-1 after brain trauma. Methods By a wing Feeney animal model,Wistar rats were divided randomly into 11 groups:dexamethasone treatment,ICAM-1 monoclone antibody(MoAb)treatment,sham operation,and 30 min,3 h,6 h,1 d,3 d,5 d and 7 d groups following experimental brain injury ( n =6 for each group).Accumulation of cerebral olymorphonuclear leukocytes(PMNs) and ICAM-1 expression were determined by counting the total PMNs or positive immunostained microvessels in two high-power field(400×)under a light microscope.The effects of dexamethasone and ICAM-1 MoAb treatment were assessed.Statistical analysis was performed using a software program(SPSS).Differences between groups were evaluated by using analysis of one-way variance.A value of P 0 05 was considered significant. Result The expression of ICAM-1 and the infiltration of RMNs increased significantly at 6 hours after injury ( P 0 05),reaching peak at postoperative day 2 and then gradually decreasing.Dexamethasone can significantly supressed the expression of ICAM-1 protein and the infiltration of PMNs ( P 0 05), while ICAM-1 MoAb has no significant influence on them ( P 0 05). Conclusion The expression of ICAM-1 and the infiltration of PMNs increase significantly following brain trauma.The time course and distribution of the expression of ICAM-1 were corresponded to the secondary damage after brain injury.These findings strongly suggest that the upregulation of ICAM-1 is involved in the secondary insult after brain trauma.