| Project/Area Number |
24590317
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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 | Nagoya University |
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Principal Investigator |
ISHIGURO Kazuhiro 名古屋大学, 医学(系)研究科(研究院), 特任准教授 (60432275)
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| Co-Investigator(Kenkyū-buntansha) |
ANDO Takafumi 名古屋大学, 大学院医学系研究科, 准教授 (80378041)
GOTO Hidemi 名古屋大学, 大学院医学系研究科, 教授 (10215501)
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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 / サイトカイン / ケモカイン / 生薬 / 腸炎 / 腸内細菌 |
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| Outline of Final Research Achievements |
1) We demonstrated the anti-inflammatory effect of Atractylodin, a gredient of atractylodes lancea rhizome, in a mouse model of colitis. Atractylodin reduced IL-17 production through the suppression of Th17 differentiation by reducing the production of IL-6, one of important cytokines involved in Th 17 differentiation. We also found that Atractylodin inhibited the binding bewtween NF-kB and IL-6 promoter on genomic DNA without affecting activation of NF-kB itself.
2) Acetate, a major short-chain fatty acid produced by gut flora, suppressed IL-8 production via the acetylation of tubulin alpha in flagellin-stimulated epithelial cells of the colonic mucosa. We proved that tubulin alpha acetylation leaded to the inhibition of Rap1 activation downstream of flagellin stimulation, resulting in the reduced expression of c-fos, a constituent of AP-1 transcription factor, which is important for IL-8 mRNA expression.
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