The molecular mechanism of aminoguanidine-mediated reduction on the brain edema after surgical brain injury in rats.

The study investigated the effect of aminoguanidine (AG) on inducible nitric oxide synthase (iNOS), aquaporin-4 (AQP4), malondialdehyde (MDA) and glutathione (GSH) levels in surgical brain injury (SBI) in rats. AG (75, 150 and 300 mg/kg, i.p.) was administered immediately following surgical resection. Using an SBI model, the absence of iNOS protein in any brain tested (sham-operated group, SBI group and SBI+AG group) at 24 h after SBI was confirmed by Western blot analysis. The expression of AQP4 protein in brain tissue at the edge of the resection site increased at 24 h after SBI, which could be greatly attenuated by the treatment with AG (150 mg/kg), while AG at the dose of 75 mg/kg or 300 mg/kg had no significant effect on it. In addition, there was a marked decrease of MDA values and a great increase of the GSH levels at 24 h after SBI in SBI+AG (150 mg/kg) group compared with SBI group. Whereas AG (300 mg/kg) elevated oxidative stress compared with SBI group. Our results indicate that the anti-edematous effect of AG observed in our study is dose-dependent and unlikely related to its inhibition effect on iNOS and may attribute to its roles on the regulation of AQP4 expression and antioxidative property at brain tissue after SBI.