| Project/Area Number |
15K19353
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Tokai University |
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Principal Investigator |
IMAI Jin 東海大学, 医学部, 助教 (40725363)
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| Co-Investigator(Renkei-kenkyūsha) |
HOZUMI Katsuto 東海大学, 医学部, 教授 (30246079)
INAGAKI Yutaka 東海大学, 医学部, 教授 (80193548)
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| Research Collaborator |
MINE Tetsuya 東海大学, 医学部, 教授 (20157572)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | クローン病 / 炎症性腸疾患 / 腸管線維化 / TGF-β / YB-1 / 線維化 |
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| Outline of Final Research Achievements |
We have previously shown that the administration of a small compound, HSc025, which promotes the nuclear translocation of YB-1 as a downstream effector of IFN-g and antagonizes TGF-b/Smad signaling, improves fibrosis in several murine tissues. In this study, we evaluated the anti-fibrotic effect of HSc025 on colorectal fibrosis in TNBS-induced murine chronic colitis. Daily oral administration of HSc025 suppressed collagen production and decreased the severity of colorectal fibrosis in a dose-dependent manner. In addition, the local production of TGF-b was decreased after HSc025 treatment. HSc025 administration maintained the level of IFN-g production, even at a late stage when IFN-g production was lost without the drug treatment. These results demonstrate that HSc025 could be a therapeutic candidate for intestinal fibrosis in inflammatory bowel disease that acts by altering the local production of cytokines, as well as by directly suppressing collagen production..
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