| Project/Area Number |
25430063
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SHIMOHATA Takayoshi 新潟大学, 脳研究所, 准教授 (60361911)
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| Co-Investigator(Renkei-kenkyūsha) |
KANAZAWA Masato 新潟大学, 医歯学総合病院, 助教 (80645101)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | アンギオポエチン1 / 脳虚血 / 脳塞栓モデル / 血管保護 / アンギオポエチン |
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| Outline of Final Research Achievements |
An angiogenesis factor, angiopoietin-1 (Ang1), is associated with the blood-brain barrier (BBB) disruption after focal cerebral ischemia. We hypothesized that administering Ang1 might attenuate hemorrhagic transformation and cerebral edema after tissue plasminogen activator (tPA) treatment by stabilizing blood vessels and inhibiting hyperpermeability. We used the rat thromboembolic focal cerebral ischemia model treated with tPA after ischemia with recombinant Ang1 protein or vehicle. Ang1 expression levels and Ang1-positive vessel densities on the ischemic side of the cerebral cortex were decreased after ischemia. Administration of recombinant Ang1 protein showed that the suppression of hemorrhagic transformation and less cerebral edema, as compared to administering vehicle protein. In conclusion, Ang1 might be a promising target molecule for developing vasoprotective therapies for controlling hemorrhagic transformation and cerebral edema after tPA treatment.
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