RESUMO
Objective This study was designed to determine the influence of acute ethanol intoxication (AEI) on brain edema and aquaporin-4(AQP-4) levels after traumatic brain injury(TBI) in rots. The underlying mechanism was also investigated. Method Severe traumatic brain injury models were made using the Feeny method; acute ethanol intoxication models were established by gavagy. One hundred and ninety-two male SD rats were randomly divided(random number) into four groups, namely the sham operation group(A ), the acute ethanol intoxication group( B ), the traumatic brain injury group(C) and the combination of acute ethanol intoxication with traumatic brain injury group(D). Each group was further divided into four sub-groups according to the time interval between injury and death of the rats. After brain tissue was fixed by affusing paraformaldehyde, the expression of AQP-4 was detected by immunohistochemistry. Water content was detected by dry-wet analysis, and AQP-4 mRNA and protein were detected by RT-PCR and western blotting respectively after the brain tissue was got by rapid decapitation. Data were analyzed by one-way ANOVA. Results The water content of brain tissue and expression level of AQP-4 were not significantly different between groups A and B( P > 0.05); however both were significantly increased in groups C and D relative to group A( P < 0.05). The water content of brain tissue in group D increased by mere than that in group C( P < 0.05), while the expression level of AQP-4 in group D was lower than that in group C(P<0.05). Conclusions Acute ethanol intoxication inhibited the expression of AQP-4,which induced a more severe cerebral edema after traumatic brain injury.