Multiple comparative analysis of FXR-inhibitory effect on liver carcinogenesis
| Project/Area Number |
26870501
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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 |
Biological pharmacy
Pathological medical chemistry
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| Research Institution | Osaka City University |
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Principal Investigator |
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| Research Collaborator |
IKEDA Kazuo
KAWADA Norifumi
TERANISHI Yuga
ODAGIRI Naoshi
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | FXR / 肝星細胞 / 肝硬変 / 肝がん / 胆汁酸受容体 / 胆汁酸 / 細胞老化 / 慢性肝炎 |
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| Outline of Final Research Achievements |
In this study, a molecular analysis of Farnesoid X receptor (FXR)-inhibitory effects in HSC activation was performed, to unveil a molecular mechanism by which liver cirrhosis induces liver carcinogenesis. Hepatic stellate cells (HSCs) were found to express FXR more highly than the other liver component cells. Lithocholic acid showed suppression of human HSC activation among major bile acids (cholic acid, chenodeoxycholic acid, deoxycholic acid, ursodeoxycholic acid). A synthetic FXR activator GW4064 also showed the suppression of human HSC activation, but another synthetic FXR activator obeticholic acid did not. These results may suggest plural pathways (or forms) of the FXR activation, although a detailed study is required.
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Report
(5 results)
Research Products
(12 results)
