| Project/Area Number |
25460378
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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 |
Pathological medical chemistry
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YAZAWA Takashi 旭川医科大学, 医学部, 講師 (00334813)
TAKEUCHI Masayuki 旭川医科大学, 医学部, 助教 (40226999)
KATOH Tsuyoshi 旭川医科大学, 医学部, 准教授 (60194833)
UWADA Junsuke 旭川医科大学, 医学部, 助教 (70580314)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | focal adhesion kinase / intestinal barrier / muscarinic cholinoceptor / 炎症性腸疾患 / 上皮バリア / focal adhesion kinase / MAP kinase / ムスカリン受容体 / acetylchoine / acetylcholine |
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| Outline of Final Research Achievements |
Tumor necrosis factor alpha (TNF) induced the reduction of TER in HT-29/B6 monolayers which was attenuated by acetylcholine or charbacol treatment. This attenuation was cancelled by the addition of atropine. TNF-induced activation of NF-kB system was inhibited by acetylcholine or charbacol treatment. This inhibition was also suppressed by the addition of atropine. TNF induced increase in the expression of inflammatory genes such as COX-2 and IL-8 genes and the excretion of IL-8 in the culture medium which were attenuated by charbacol treatment. This attenuation was also cancelled by the addition of atropine.
These results suggest that muscarinic signaling system may enforce intestinal epithelial barrier function against inflammatory barrier disruption and may prevent inflammatory expansion at the same time.
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