| Project/Area Number |
26461919
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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 surgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
Kamohara Hidenobu 熊本大学, 大学院生命科学研究部(医), 准教授 (90398222)
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| Co-Investigator(Kenkyū-buntansha) |
木下 順弘 熊本大学, 大学院生命科学研究部(医), 教授 (30195341)
鷺島 克之 熊本大学, 医学部附属病院, 助教 (40336235)
田代 貴大 熊本大学, 医学部附属病院, 非常勤診療医師 (00613340)
新森 大佑 熊本大学, 医学部附属病院, 診療助手 (70635789)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | neutrophil / CXCL-8 / CXCL-1 / CXCL-2 / SIRS / cellular trafficking / Rab / CXCR1/2 / CXCL8 / CXCR1 / CXCR2 / 好中球 / 細胞内輸送 / 細胞遊走 |
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| Outline of Final Research Achievements |
NeNeutrophils migration is the early process of systemic inflammatory response by SIRS. Curcumin, an inhibitor of NF-kappa B, inhibits neutrophils migration in a dose dependent manner. In this study, it depended on the recovery (recycle) on the surface of CXCR-1/2 which was a receptor of CXCL-8. Its recycling activity of CXCR-1/2 was suppressed by Curcumin. Although the binding of CXCL-8 and CXCR-1/2 was internalized and desensitized in endosome. Rab-11 which was the intracellular transport protein bound to CXCR-1/2. Rab-11 contributed to the recycle regulation of CXCR-1/2. These results suggested that intracellular trafficking molecules could be novel targets in treatment of SIRS.
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