| Project/Area Number |
25670022
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Biological pharmacy
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| Research Institution | University of Toyama |
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Principal Investigator |
KOIZUMI Keiichi 富山大学, 和漢医薬学総合研究所, 准教授 (10334715)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ケモカイン / CXCL16 / NASH / NKT / 肥満 / 欠損マウス |
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| Outline of Final Research Achievements |
NASH (nonalcoholic steatohepatitis) is a serious disease, which goes to liver cirrhosis and liver cancer. However, NASH progression mechanism is still unknown. Recently, we interestingly found a NASH-inducing transplanted NKT into the recipient of NKT cell-deficient mice. The purpose of this study is following two; 1.Analysis of the immunological function of the NKT cells. 2.Development of the new drug against NASH. As a result of our investigation, initial condition of NASH was observed by taking of CDAA diet for 2-weeks in CXCL16-deficient mice. Furthermore, it was clear that IFN-γ and TNF-α produced from hepatic mononuclear cells by the NKT cells is a effector molecule for lipid accumulation in liver cells.
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