| Project/Area Number |
18K08654
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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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| Review Section |
Basic Section 55020:Digestive surgery-related
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| Research Institution | Osaka City University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
南山 幸子 京都府立大学, 生命環境科学研究科, 教授 (00362989)
久保 正二 大阪市立大学, 大学院医学研究科, 准教授 (80221224)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 非アルコール性脂肪性肝炎 / 線維化 / アリルシステイン / セラミド / 脂肪性肝炎 / 肝線維化 / 非アルコール性脂肪性肝疾患 / バイオマーカー / マクロファージ |
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| Outline of Final Research Achievements |
In this study, we investigated the effect of S-allyl glutathione (SAG) on the progression of NAFLD/NASH via suppression of macrophage polarization. First, we were able to induce NAFLD by high-fat diet using a rat NAFLD model that is more in line with clinical conditions. As a result of quantitative analysis of ceramide in the liver, there was no difference in the total amount of ceramide between the various groups. On the other hand, the percentage of specific ceramide molecular species was found to be highly variable in NAFLD. Histologically, the fat droplets in the hepatocytes were reduced in size after SAG treatment. At the same time, we confirmed that SAG treatment reduced pro-inflammatory and anti-inflammatory cytokines and caused a significant decrease in fibrosis markers.
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| Academic Significance and Societal Importance of the Research Achievements |
低分子化合物であるSAGは、マクロファージの分極制御を介してNAFLDにおける炎症応答を軽減し、筋線維芽細胞の活性化を制御、線維化を改善することによってNAFLD病態を改善する作用を有することが判明した。一方、脂質組成に影響されるセラミドの分子種をNAFLDの病態のバイオマーカーとする可能性が確認されたがその詳細はさらなる検討が必要である。
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