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ID 63225
フルテキストURL
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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 ORCID Kaken ID publons researchmap
Munemasa, Shintaro Graduate School of Environmental and Life Science, Okayama University ORCID
Murata, Yoshiyuki Graduate School of Environmental and Life Science, Okayama University ORCID Kaken ID publons researchmap
Nakamura, Toshiyuki Graduate School of Environmental and Life Science, Okayama University
Nakamura, Yoshimasa Graduate School of Environmental and Life Science, Okayama University ORCID Kaken ID publons researchmap
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.
キーワード
3-hydroxyphenylacetic acid
aldehyde dehydrogenase
quercetin metabolites
aryl hydrocarbon receptor
acetaldehyde
発行日
2022-02-03
出版物タイトル
International Journal Of Molecular Sciences
23巻
3号
出版者
MDPI
開始ページ
1762
ISSN
1422-0067
NCID
AA12038549
資料タイプ
学術雑誌論文
言語
英語
OAI-PMH Set
岡山大学
著作権者
© 2022 by the authors.
論文のバージョン
publisher
PubMed ID
DOI
Web of Science KeyUT
関連URL
isVersionOf https://doi.org/10.3390/ijms23031762
ライセンス
https://creativecommons.org/licenses/by/4.0/