Reduced brain edema after traumatic brain injury in mice deficient in P-selectin and intercellular adhesion molecule-1.

摘要: Platelet (P-) selectin and intercellular adhesion molecule-1 (ICAM-1) mediate accumulation of neutrophils in brain. However, the mechanisms regulating neutrophil damage after traumatic brain injury (TBI) are poorly defined. We hypothesized that mice deficient both P-selectin ICAM-1 (-/-) would have decreased edema, improved functional histopathological outcome TBI compared with wild-type (+/+). In Protocol I, water content were quantified at 24 h TBI. No difference was observed between groups; however, edema dual -/- (P < 0.05 vs. +/+ mice). II, TBI, tests motor memory function histopathology assessed over 21 days. or mice. A role for molecules pathogenesis independent leukocyte is suggested.