| Project/Area Number |
24659376
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Tokai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ISHII Naoaki 東海大学, 医学部, 教授 (60096196)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 酸化ストレス / 肝線維化 / マクロファージ / 非アルコール性脂肪肝炎 / 肝線維症 / コラーゲン遺伝子 |
|---|
| Research Abstract |
Oxidative stress is considered to play a key role in the progression of chronic liver diseases. However, since production of oxidative stress may merely represent the consequences of cell damage and subsequent inflammation, it is virtually unknown whether oxidative stress is linked directly to fibrogenesis.
Hepatocytes isolated from Tet-mev-1 mouse, in which mitochondrial reactive oxygen species can be induced, exhibited decreased mitochondrial membrane potential. Tet-mev-1 mice were fed high fat/high sucrose (HFHS)diet, and microarray analyses indicated that CC chemokine expression was remarkably elevated in the liver tissue. However, the number of F4/80-positive cells was substantially decreased, and there was no
apparent liver fibrosis observed in Tet-mev-1 mice fed HFHS diet. These results suggested the important role of macrophages in the progression of liver fibrosis.
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