Involvement of redox mechanisms in ischemic neuronal death

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We investigated the role of redox mechanisms in ischemic neuronal damage in rodent models. Cerebral ischemia (transient occlusion of middle cerebral artery with thread) and mitochondrial impairment (by systemic administration of 3-nitropropionic acid) up-regulated thioredoxin (TRX) and its mRNA in neurons of rat brain, and mutant mice with overexpression of TRX showed significant resistance to ischemic insults and excitotoxic neuronal damages compared with wild ones. Systemic administration of TRX just after the onset of ischemic insult for 3 hours significantly reduced cerebral infarct volume in mice. In hypoxia-ischemia model of rat neonates (unilateral common carotid artery occlusion+8% hypoxia for 2 hours), TRX was strongly detected in cerebral cortex and hippocampus. These results imply that TRX acts as a neuroprotective molecule in various rodent cerebral ischemic models and may serve as a new therapeutic agent against ischemic neuronal damage in human.