| Project/Area Number |
21590271
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | University of Toyama |
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Principal Investigator |
YOKOO Hiroki 富山大学, 大学院・医学薬学研究部(医学), 准教授 (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)
YAMAMOTO Seiji 富山大学, 大学院・医学薬学研究部(医学), 助教 (10456361)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 炎症 / 免疫 / 敗血症 / 酸化ストレス / ニトロ化ストレス / Akt / インスリン作用不全 / NADPH oxidase活性 / ラジカルスカベンジャー / 細胞委縮変形像 / インスリンシグナル / PI3K-Akt / 細胞濃染色像 / 細胞萎縮変形像 / リモデリング / スタチン / 核濃染色 / 核委縮 |
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| Research Abstract |
We analyzed the insulin signal in septicemia, using the brain and lung tissue in septic model mice. Until the certain period, insulin signal was increased by some defensive mechanisms. However, the signal was reduced gradually, and the degree of tissue damage was increased. Meanwhile, treatment the drugs which maintain the signal reduced the tissue damage. It was expected that the damage in septicemia would be reduced, if we use the protective system via insulin signal, which reduce the oxidative and nitrative stress.
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