ID | 63225 |
フルテキストURL | |
著者 |
Liu, Yujia
School of Biological Engineering, Dalian Polytechnic University
Myojin, Takumi
Graduate School of Environmental and Life Science, Okayama University
Li, Kexin
Graduate School of Environmental and Life Science, Okayama University
Kurita, Ayuki
Graduate School of Environmental and Life Science, Okayama University
Seto, Masayuki
Graduate School of Environmental and Life Science, Okayama University
Motoyama, Ayano
Graduate School of Environmental and Life Science, Okayama University
Liu, Xiaoyang
Graduate School of Environmental and Life Science, Okayama University
Satoh, Ayano
Graduate School of Interdisciplinary Science and Engineering in Health Systems, Okayama University
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Munemasa, Shintaro
Graduate School of Environmental and Life Science, Okayama University
ORCID
Murata, Yoshiyuki
Graduate School of Environmental and Life Science, Okayama University
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Nakamura, Toshiyuki
Graduate School of Environmental and Life Science, Okayama University
Nakamura, Yoshimasa
Graduate School of Environmental and Life Science, Okayama University
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抄録 | Aldehyde dehydrogenases (ALDHs) are the major enzyme superfamily for the aldehyde metabolism. Since the ALDH polymorphism leads to the accumulation of acetaldehyde, we considered that the enhancement of the liver ALDH activity by certain food ingredients could help prevent alcohol-induced chronic diseases. Here, we evaluated the modulating effects of 3-hydroxyphenylacetic acid (OPAC), the major metabolite of quercetin glycosides, on the ALDH activity and acetaldehyde-induced cytotoxicity in the cultured cell models. OPAC significantly enhanced the total ALDH activity not only in mouse hepatoma Hepa1c1c7 cells, but also in human hepatoma HepG2 cells. OPAC significantly increased not only the nuclear level of aryl hydrocarbon receptor (AhR), but also the AhR-dependent reporter gene expression, though not the nuclear factor erythroid-2-related factor 2 (Nrf2)-dependent one. The pretreatment of OPAC at the concentration required for the ALDH upregulation completely inhibited the acetaldehyde-induced cytotoxicity. Silencing AhR impaired the resistant effect of OPAC against acetaldehyde. These results strongly suggested that OPAC protects the cells from the acetaldehyde-induced cytotoxicity, mainly through the AhR-dependent and Nrf2-independent enhancement of the total ALDH activity. Our findings suggest that OPAC has a protective potential in hepatocyte models and could offer a new preventive possibility of quercetin glycosides for targeting alcohol-induced chronic diseases.
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キーワード | 3-hydroxyphenylacetic acid
aldehyde dehydrogenase
quercetin metabolites
aryl hydrocarbon receptor
acetaldehyde
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発行日 | 2022-02-03
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出版物タイトル |
International Journal Of Molecular Sciences
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巻 | 23巻
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号 | 3号
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出版者 | MDPI
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開始ページ | 1762
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ISSN | 1422-0067
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NCID | AA12038549
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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著作権者 | © 2022 by the authors.
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.3390/ijms23031762
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ライセンス | https://creativecommons.org/licenses/by/4.0/
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