| Project/Area Number |
26461278
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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 |
Neurology
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| Research Institution | Saitama Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
丸山 元 埼玉医科大学, 医学部, 助教 (00646680)
福岡 卓也 埼玉医科大学, 医学部, 講師 (50646221)
栗田 浩樹 埼玉医科大学, 医学部, 教授 (70262003)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2016: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 脳虚血 / 微小循環障害 / 再灌流 / アンギオテンシン |
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| Outline of Final Research Achievements |
Deranged microcirculation is one of the reasons of unsatisfactory results of thrombolytic therapy for ischemic stroke. We investigated role of angiotensin for the microcirculation disturbance in the ischemic brain.
With use of type 1 angiotensin II receptor (AT1) knock-out and wld-type mice, we observed adhesion and rolling of leukocytes and platelets on the microvessel wall in the brain after transient ischemia. Fewer numbers of cells showed adhesion and rolling in the AT1 knock-out mice. Then we used type 2 angiotensin II receptor (AT2) knock-out and wld-type mice, and observed in a same manner. Contrarilly, AT2 knock-out mice showed more adhesion and rolling of leukocytes and platelets in the brain microvessels after transient ischemia.
Blocking AT1 and stimulation of AT2 are associated with better prognosis in human stroke. Our results indicate that improved microcirculation could underlie this brain-protective effect.
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