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language
eng
Author
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
Katakura, Masanori
Hashimoto, Michio
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
Description
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.
Journal Title
Scientific Reports
Volume
10
Start Page
15553
ISSN(Online)
2045-2322
Published Date
2020-9-23
DOI
Publisher
Springer Nature
NII Type
Journal Article
OAI-PMH Set
Faculty of Medicine