2013 Fiscal Year Final Research Report
Protective effects of angiotensin receptor control on ischemic neuronal injury
| Project/Area Number |
23592083
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 |
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| Co-Investigator(Kenkyū-buntansha) |
SUGAWARA Taku 秋田大学, 医学部, 講師 (80241660)
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| Project Period (FY) |
2011 – 2013
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| Keywords | アンジオテンシン受容体 / 脳虚血 / 神経細胞死 / アポトーシス |
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| Research Abstract |
Mitochondrial apoptosis after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type 1 receptor activation results in production of superoxide, but whether angiotensin II type 1 receptor blockade prevents mitochondrial apoptosis after ischemia remains unclear. Normotensive rats received the angiotensin II type 1 receptor blocker, candesartan or only vehicle before induction of global cerebral ischemia. Approximately 30% of the hippocampal CA1 neurons survived in candesartan-treated animals, whereas only 2% of neurons survived in vehicle-treated animals. Superoxide production and cytochrome c release were significantly less in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. Angiotensin II type 1 receptor may have an essential role in apoptotic cell death in vulnerable neurons after global cerebral ischemia.
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