Amelioration of ischemic neuronal by angiotensin receptor control
Project/Area Number |
18591574
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
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Research Institution | Akita University |
Principal Investigator |
SUGAWARA Taku Akita University, Akita University School of Medicine, Lecturer (80241660)
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Project Period (FY) |
2006 – 2007
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Project Status |
Completed (Fiscal Year 2007)
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Budget Amount *help |
¥3,890,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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Keywords | global cerebral ischemia / hippocampal neurons / apoptosis / oxidative stress / superoxide / angiotensin II / DNA損傷 / 海馬CA1領域 / アンジオテンシン受容体 |
Research Abstract |
Excessive superoxide production 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 production of superoxide and subsequent neuronal injury 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 was 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 superoxide production and subsequent injury in vulnerable neurons after global cerebral ischemia.
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Report
(3 results)
Research Products
(11 results)
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[Journal Article] Direct correlation between ischemic injury and extracellular glycine concentration in mice with genetically altered activities of the glycine cleavage multienzyme system2007
Author(s)
Oda M, Kure S, Sugawara T, Yamaguchi S, Kojima K, Shinka T, Sato K, Narisawa A, Aoki Y, Matsubara Y, Omae T, Mizoi K, Kinouchi H.
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Journal Title
Stroke 38
Pages: 2157-2164
Related Report
Peer Reviewed
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