| Project/Area Number |
10470291
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
HASHIMOTO Nobuo Kyoto University, Neurosurgery, Professor, 医学研究科, 教授 (40135570)
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| Co-Investigator(Kenkyū-buntansha) |
NOZAKI Kazuhiko Kyoto University, Neurosurgery, Assistant Professor, 医学研究科, 講師 (90252452)
宝子丸 稔 京都大学, 大津市民病院脳神経外科
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥11,800,000 (Direct Cost: ¥11,800,000)
Fiscal Year 2000: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1999: ¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 1998: ¥5,200,000 (Direct Cost: ¥5,200,000)
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| Keywords | Cerebral ischemia / Redox / Thioredoxin / Cerebral infection / neuron / Cerebral ischemia / redox / Thioredoxin / cerebral infarction / redox regulation / oxidative stress / cerebral ischemia / thioredoxin / rat / mouse / ラット / ジャービル |
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| Research Abstract |
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.
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