To investigate the effect of vitamin C (VitC) on reducing secondary brain injury caused by traumatic brain injury (TBI) after alcohol consumption and its possible mechanism.

Rats were randomly assigned into TBI+only group, TBI+EtOH group, TBI+VitC group and TBI+EtOH+VitC group, 10 rats in each group. TBI model was established, and 24 h after TBI, the neurological injury score, brain water content and Evans blue content were measured. Western blot was used to evaluate the expressions of P450 (CYP2E1), AQP-4, MMP-9 and Occludin in the tissue of the damaged brain 24 h after TBI with alcohol consumption.

After 24 h of percussion, the neurological injury score, brain water content and Evans blue content of TBI+EtOH group were significantly increased, after VitC intervention, the indexes were significantly reduced, the difference among the groups was statistically significant (P<0.05); compared with TBI+EtOH group, the expression of CYP2E1, AQP-4 and MMP-9 were decreased, the content of occludin was increased, and the difference between the groups was statistically significant (P<0.05).

Acute ethanol intake aggravates cytotoxic brain edema after TBI, while VitC can reduce the activation of AQP-4 and MMP-9 through CYP2E1, increase the expression of occludin protein, reduce the breakdown of tight connection of blood-brain barrier and the destruction of integrity, reduce the opening of blood-brain barrier and reduce brain edema, and ultimately improve neurological function.