| Project/Area Number |
16591428
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Akita University |
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Principal Investigator |
SUGAWARA Taku Akita University, School of Medicine, Assistant Professor, 医学部, 講師 (80241660)
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| Co-Investigator(Kenkyū-buntansha) |
KINOUCHI Hiroyuki Yamanashi University, School of Medicine, Professor, 大学院・医学工学総合研究部, 教授 (30241623)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | global cerebral ischemia / superoxide / angiotensin receptor / angiotensin II / アポトーシス / 海馬CA1領域 |
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| Research Abstract |
Excessive superoxide production after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type 1 receptor (AT1R) activation is recently identified as a source of superoxide, however, it has not been clear whether blockade of AT1R leads to reduction of superoxide and subsequent neuronal injury after ischemia. Normotensive rats received AT1R blocker, candesartan or vehicle and subjected to global cerebral ischemia. Candesartan rescued approximately 30% of the hippocampal CA1 neurons, whereas only 2% of neurons survived in vehicle-treated animals. There was significantly less superoxide production in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. AT1R may play a pivotal role in superoxide production and subsequent injury in the vulnerable neurons after global cerebral ischemia.
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