言語 |
英語
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著者 |
Toko, Haruhiro
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Morita, Hiroyuki
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
片倉 賢紀
橋本 道男
Ko, Toshiyuki
Bujo, Satoshi
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Adachi, Yusuke
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Ueda, Kazutaka
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Murakami, Haruka
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Ishizuka, Masato
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Guo, Jiaxi
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Zhao, Chunxia
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Fujiwara, Takayuki
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Hara, Hironori
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Takeda, Norifumi
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Takimoto, Eiki
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Harada, Mutsuo
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
Komuro, Issei
Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo
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内容記述(抄録等) | Some clinical trials showed that omega-3 fatty acid (FA) reduced cardiovascular events, but it remains unknown whether omega-3 FA supplementation changes the composition of FAs and their metabolites in the heart and how the changes, if any, exert beneficial effects on cardiac structure and function. To clarify these issues, we supplied omega-3 FA to mice exposed to pressure overload, and examined cardiac structure and function by echocardiography and a proportion of FAs and their metabolites by gas chromatography and liquid chromatography-tandem mass spectrometry, respectively. Pressure overload induced cardiac hypertrophy and dysfunction, and reduced concentration of all FAs’ components and increased free form arachidonic acid and its metabolites, precursors of pro-inflammatory mediators in the heart. Omega-3 FA supplementation increased both total and free form of eicosapentaenoic acid, a precursor of pro-resolution mediators and reduced free form arachidonic acid in the heart. Omega-3 FA supplementation suppressed expressions of pro-inflammatory cytokines and the infiltration of inflammatory cells into the heart and ameliorated cardiac dysfunction and fibrosis. These results suggest that omega-3 FA-induced changes of FAs composition in the heart have beneficial effects on cardiac function via regulating inflammation.
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掲載誌名 |
Scientific Reports
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巻 | 10
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開始ページ | 15553
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ISSN(Online) | 2045-2322
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発行日 | 2020-9-23
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DOI | |
出版者 | Springer Nature
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資料タイプ |
学術雑誌論文
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部局 |
医学部
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