Analysis of cytotoxic signal pathway in organ dysfunctions associated with sepsis
| Project/Area Number |
21592304
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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 |
Emergency medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
CHOU Kyouhiro 東京大学, 医学部附属病院, 講師 (50302708)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Yoshitsugu 東京大学, 医学部附属病院, 教授 (30166748)
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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: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 敗血症 / 細胞死 / アポトーシス / 多臓器不全 / 一酸化窒素 / 酸化ストレス / MAP kinase / 抗酸化薬 / 炎症性メディエーター / 急性尿細管障害 |
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| Research Abstract |
To elucidate the pathophysiology of organ dysfunction associated with sepsis, we have analyzed cytotoxicity induced by proinflammatory cytokines in various cultured cell lines.
A mixture of proinflammatory cytokines exerted synergistic cytotoxic effects and this cytotoxicity was mediated at least partially by the caspase-dependent apoptotic signaling pathway.
The profile of cytotoxicity differed according to cell types, in terms of nitric oxide or MAP kinase dependency.
Antiinflammatory agents or antioxidants showed prominent cytoprotective effects against the cytotoxicity induced by proinflammatory cytokines.
Cell death other than apoptosis was implied in the underlying mechanism of the cytotoxicity induced by proinflammatory cytokines.
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Report
(4 results)
Research Products
(18 results)
