The present study examined the effects of a selective inducible nitric oxide synthase inhibitor, aminoguanidine (AG) on neuronal cell survival after middle cerebral artery occlusion (MCAO) in hippocampal CA1 region. Transient focal cerebral ischemia was induced in rats by 60 min MCAO, followed by 7 days of reperfusion. Saline as vehicle or AG at the dosage of 150 mg/kg i.p. was administered immediately after occlusion and thereafter twice a day for three days. The evaluation of infarcted volume was made by 2,3,5-triphenyltetrazolium chloride (TTC). For comparison of cellular viability we used Fluoro-Jade B and NeuN staining to examine the evolving phases of infarction induced by MCAO. Treatment with AG signifi cantly reduced total infarct volumes by 55% in comparison with saline group. AG signifi cantly improved the neurological outcome. The number of degenerating neurons was markedly reduced in hippocampal CA1 region compared to groups without AG treatment. These changes were seen in the ipsilateral and contralateral hippocampus. In conclusion, the focal ischemia affects the hippocampus, which responds bilaterally to the injury. Our fi ndings show that AG decreases ischemic brain damage and improves neurological recovery after transient ischemia induced by MCAO. It is suggested that treatment with AG may present a potential therapeutic strategy for the treatment of traumatic brain injury. This study was supported by VEGA 2/0141/09, VEGA 2/0146/09, VEGA 1/4237/07 and APVV LPP 0235-06.
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