| Project/Area Number |
15K09316
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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 | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
太田 康之 岡山大学, 大学病院, 講師 (20746854)
菱川 望 岡山大学, 大学病院, 助教 (90378175)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 脳血管障害 / 低酸素ストレス / 酸化ストレス / アストロサイト / 脳梗塞 / 脳組織保護 |
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| Outline of Final Research Achievements |
In this study, we focused on the role of astrocytes in hypoxia and oxidative stress of cerebral infarction, and analyzed it using mouse focal cerebral ischemia model. Immunohistochemistry of cerebral tissue sections showed remarkable increased expression of HIF1α, a hypoxic stress marker, around the cerebral infarction lesions 12 hours after the cerebral infarction, and the highest expression of GSH, antioxidant stress marker, 72 hours after the onset of cerebral infarction. In vivo imaging and on immunohistochemical analyses, the expression of Nrf2, an oxidative stress marker, peaked after 24 hours, and Nrf2 was expressed in both neurons and astrocytes. This study suggested that hypoxic stress was first involved in cerebral infarction, then oxidative stress was involved, in which astrocyte acted mainly.
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