Role of Keap1/Nrf2 system in host defense against acute lung injury.
| Project/Area Number |
20590911
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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 |
Respiratory organ internal medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
ISHII Yukio University of Tsukuba, 大学院・人間総合科学研究科, 准教授 (80272194)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | Nrf2 / Keap1 / 酸化ストレス / 急性肺傷害 / マクロファージ / 転写因子 / 肺線維症 / Th1/Th2 / Th1 / Th2 / 敗血症 / 急性呼吸促迫症候群 / リポ多糖体 / Toll様受容体 |
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| Research Abstract |
In the present study, we investigated the role of Nrf2 in protection against the development of acute lung injury. Mice lacking Nrf2 were susceptible to acute lung injury induced by several stimuli, such as bleomycin, lipopolysaccaride, and influenza virus. The induction of several self-defense genes was lower in the lungs of Nrf2-deficient mice than in wild-type mice. Activation of nuclear factor-κB and induction of proinflammatory cytokines were significantly higher in Nrf2-deficient mice than in wild-type mice. Results indicate Nrf2 is a pivotal factor in protection against the development of acute lung injury induced by environmental stimuli.
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Report
(4 results)
Research Products
(19 results)
