| Project/Area Number |
24590315
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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 |
General pharmacology
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| Research Institution | Tokoha University (2014)
University of Toyama (2012-2013) |
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Principal Investigator |
YOKOO Hiroki 常葉大学, 健康プロデュース学部, 教授 (30332894)
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| Co-Investigator(Kenkyū-buntansha) |
HATTORI Yuichi 富山大学, 大学院医学薬学研究部(医学), 教授 (50156361)
TAKANO Yasuo 東京工科大学, 医療保健学部, 教授 (60142022)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 炎症 / 酸化ストレス / 敗血症 / NADPH oxidase / 酸化/ニトロ化ストレス / 活性酸素 / ラジカルスカベンジャー / 細胞委縮変形像 / 高濃度グルコース / HMGB1 / ルシゲニン / 高グルコース |
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| Outline of Final Research Achievements |
We focused on NADPH oxidase (Nox) activity and studied about sepsis encephalopathy. Proinflammatory cytokines and brain vessel permeability were significantly up-regulated in septic mice brain. And, Nox subunits, p47phox and p67phox, oxidative stress marker 8-OHdG, and iNOS expression were up-regulated in septic brains. These indicate that superoxide, produced by Nox, reacts with NO to form peroxynitrite, that might provoke a failed blood brain barrier. Light and electron microscopic examination showed that serious neuronal degeneration was occurred in septic mice brain. However, these histopathological changes were mitigated by treatment with the free radical scavenger edaravone. Thus, it was suggested that Nox gene might be therapeutic target for treating septic encephalopathy.
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