| Project/Area Number |
25893280
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Pain science
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| Research Institution | Hyogo University of Health Sciences |
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Principal Investigator |
WANG Shenglan 兵庫医療大学, 薬学部, 助教 (50714359)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 内臓痛 / DSSモデル / TNBSモデル / TRPチャネル / 免疫調節因子 / TRP / IBD / DSS / TNBS / 大腸炎 |
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| Outline of Final Research Achievements |
We made two kinds of IBD rat models and detected the expression of inflammatory cytokines, pain-related receptors and oxidants in DRG neurons or colonic tissues. We found several cytokines, TRPA1 and H2O2 contents increased in DRG neuros or colonic tissues of IBD rats. Using a recording of visceromotor response to colorectal distention, we observed that the increased H2O2 sensitized TRPA1 channel to evoke visceral hyperalgesia in TNBS rats. We also evaluated interaction of colonic motility and visceral pain. We found that intrarectal administration with AITC (a TRPA1 agonist) increased both colonic motilities and visceral pain behaviors. 4-DAMP, an antagonist of acetylcholine receptors subtype M3, inhibited the AITC-induced colonic motility and visceral pain. These results indicate that the mechanism of visceral pain in IBDs involve the inflammatory cytokines, pain-related receptors, oxidants and visceral motilities, which factors are interact each other and form a complex machinery.
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