Aminoguanidine Administration Ameliorates Hippocampal Damage After Middle Cerebral Artery Occlusion in Rat
- 147 Downloads
The effects of a selective inducible nitric oxide synthase inhibitor aminoguanidine (AG) on neuronal cells survival in hippocampal CA1 region after middle cerebral artery occlusion (MCAO) were examined. Transient focal cerebral ischemia was induced in rats by 60 or 90 min of MCAO, followed by 7 days of reperfusion. AG treatment (150 mg/kg i.p.) significantly reduced total infarct volumes: by 70% after 90 min MCAO and by 95% after 60 min MCAO, compared with saline-treated ischemic group. The number of degenerating neurons in hippocampal CA1 region was also markedly lower in aminoguanidine-treated ischemic groups compared to ischemic groups without AG-treatment. The number of iNOS-positive cells significantly increased in the hippocampal CA1 region of ischemic animals, whereas it was reduced in AG-treated rats. Our findings demonstrate that aminoguanidine decreases ischemic brain damage and improves neurological recovery after transient focal ischemia induced by MCAO.
KeywordsCerebral ischemia Hippocampus Aminoguanidine iNOS
This study was supported by the VEGA 2/0141/09 and VEGA 2/0146/09 grants. This publication is the result of the project implementation: “New possibilities of preservation of neurons in the process of delayed neuronal death by nonspecific stressors” supported by the Research and Development Operational Programme funded by the ERDF. The authors gratefully acknowledge the excellent technical assistance of Dana Jurusova.