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Title:
Aminoguanidine Administration Ameliorates Hippocampal Damage After Middle Cerebral Artery Occlusion in Rat | Neurochemical Research
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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.
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article, pubmed, google, scholar, cas, cerebral, brain, aminoguanidine, ischemia, res, rat, ischemic, neuronal, middle, artery, occlusion, focal, damage, transient, rats, hippocampal, burda, nitric, oxide, stroke, research, danielisova, mcao, access, injury, neurochem, privacy, cookies, content, nemethova, effects, induced, delayed, death, hippocampus, neurosci, publish, search, ameliorates, gottlieb, inducible, synthase, region, neurons, model,
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month download article/chapter miroslava nemethova & miroslav gottlieb improves neurological recovery saline-treated ischemic group cerebral ischemia-reperfusion injury post-ischemic brain edema cerebral ischemic damage ischemia-reperfusion brain injury full article pdf nitric oxide production nitric oxide synthases related subjects fluoro-jade evident neurodegeneration enhances neurologic recovery global cerebral ischemia focal cerebral ischemia privacy choices/manage cookies hippocampal ca1 region ischemic cerebral cortex ischemic tolerance acquisition delayed neuronal death transient focal ischemia global ischemia duration creb binding protein temporary focal ischemia article danielisova aminoguanidine inhibits caspase-3 neuronal cells survival transient forebrain ischemia focal ischemia-reperfusion ischemic cell death experimental cerebral infarction transient ischemia induced delayed treatment traumatic brain injury surgical brain injury aminoguanidine ameliorates aminoguanidine involve reduced nitric oxide european economic area butler tl enzymatically formed 3-aminopropanal glial cell death luminol-enhanced chemiluminescence authors gratefully acknowledge oxidant-induced apoptosis check access instant access transient focal ischaemia conditions privacy policy
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headline:Aminoguanidine Administration Ameliorates Hippocampal Damage After Middle Cerebral Artery Occlusion in Rat
description: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.
datePublished:2011-01-04T00:00:00Z
dateModified:2011-01-04T00:00:00Z
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Hippocampus
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iNOS
Neurosciences
Neurochemistry
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Neurology
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headline:Aminoguanidine Administration Ameliorates Hippocampal Damage After Middle Cerebral Artery Occlusion in Rat
description: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.
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Hippocampus
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iNOS
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Neurology
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