2017 Fiscal Year Final Research Report
Elucidation of the mechanism of onset of fatty liver / NASH caused by oxidative stress
| Project/Area Number |
15K01736
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Applied health science
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
崎山 晴彦 兵庫医科大学, 医学部, 講師 (30508958)
江口 裕伸 兵庫医科大学, 医学部, 助教 (60351798)
吉原 大作 兵庫医科大学, 医学部, 助教 (00567266)
藤原 範子 兵庫医科大学, 医学部, 教授 (10368532)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 酸化ストレス / 抗酸化酵素 / SOD1 / NASH / 脂肪肝 / グリケーション |
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| Outline of Final Research Achievements |
SOD1 plays a protective role in cells by catalyzing the conversing of the superoxide anion into molecular oxygen and hydrogen peroxide. SOD1 is highly expressed in the liver. We measured expression level of RAGE and found that RAGE was highly expressed in SOD1 knock out (KO) mouse liver. These results suggested that oxidative stress was also accelerated by AGEs through RAGE.
SOD1 KO mice are fatty liver, resulting in liver cancer finally through fibrosis, NASH, cirrhosis of the liver with further progression. We found a higher accumulation of collagen in liver tissue from SOD1 KO mice. The level of TIMP, which is inhibitor of MMP, was also increased in SOD1 KO mice livers. These results indicate that collagen degradation is inhibited. In addition, SOD1 KO mice liver sections were modified by AGEs. These results suggest that modified collagen would be more resistant to the action of collagen degrading enzymes.
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| Free Research Field |
酸化ストレス
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