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Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression

Acetaldehyde is the major toxic metabolite of alcohol (ethanol) and enhances fibrosis of the liver through hepatic stellate cells. Additionally, alcohol administration causes the accumulation of reactive oxygen species (ROS), which induce hepatocyte injury-mediated lipid peroxidation. Iso-α-acids, c...

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Autores principales: Takase, Takahito, Toyoda, Tsudoi, Kobayashi, Naoyuki, Inoue, Takashi, Ishijima, Tomoko, Abe, Keiko, Kinoshita, Hiroshi, Tsuchiya, Youichi, Okada, Shinji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7864453/
https://www.ncbi.nlm.nih.gov/pubmed/33544749
http://dx.doi.org/10.1371/journal.pone.0246327
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author Takase, Takahito
Toyoda, Tsudoi
Kobayashi, Naoyuki
Inoue, Takashi
Ishijima, Tomoko
Abe, Keiko
Kinoshita, Hiroshi
Tsuchiya, Youichi
Okada, Shinji
author_facet Takase, Takahito
Toyoda, Tsudoi
Kobayashi, Naoyuki
Inoue, Takashi
Ishijima, Tomoko
Abe, Keiko
Kinoshita, Hiroshi
Tsuchiya, Youichi
Okada, Shinji
author_sort Takase, Takahito
collection PubMed
description Acetaldehyde is the major toxic metabolite of alcohol (ethanol) and enhances fibrosis of the liver through hepatic stellate cells. Additionally, alcohol administration causes the accumulation of reactive oxygen species (ROS), which induce hepatocyte injury-mediated lipid peroxidation. Iso-α-acids, called isohumulones, are bitter acids in beer. The purpose of this study was to investigate the protective effects of iso-α-acids against alcoholic liver injury in hepatocytes in mice. C57BL/6N mice were fed diets containing isomerized hop extract, which mainly consists of iso-α-acids. After 7 days of feeding, acetaldehyde was administered by a single intraperitoneal injection. The acetaldehyde-induced increases in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were suppressed by iso-α-acids intake. Hepatic gene expression analyses showed the upregulation of detoxifying enzyme genes, glutathione-S-transferase (GST) and aldehyde dehydrogenase (ALDH). In vitro, iso-α-acids upregulated the enzymatic activities of GST and ALDH and induced the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nfe2l2; Nrf2), a master regulator of antioxidant and detoxifying systems. These results suggest that iso-α-acid intake prevents acetaldehyde-induced liver injury by reducing oxidative stress via Nrf2-mediated gene expression.
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spelling pubmed-78644532021-02-12 Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression Takase, Takahito Toyoda, Tsudoi Kobayashi, Naoyuki Inoue, Takashi Ishijima, Tomoko Abe, Keiko Kinoshita, Hiroshi Tsuchiya, Youichi Okada, Shinji PLoS One Research Article Acetaldehyde is the major toxic metabolite of alcohol (ethanol) and enhances fibrosis of the liver through hepatic stellate cells. Additionally, alcohol administration causes the accumulation of reactive oxygen species (ROS), which induce hepatocyte injury-mediated lipid peroxidation. Iso-α-acids, called isohumulones, are bitter acids in beer. The purpose of this study was to investigate the protective effects of iso-α-acids against alcoholic liver injury in hepatocytes in mice. C57BL/6N mice were fed diets containing isomerized hop extract, which mainly consists of iso-α-acids. After 7 days of feeding, acetaldehyde was administered by a single intraperitoneal injection. The acetaldehyde-induced increases in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were suppressed by iso-α-acids intake. Hepatic gene expression analyses showed the upregulation of detoxifying enzyme genes, glutathione-S-transferase (GST) and aldehyde dehydrogenase (ALDH). In vitro, iso-α-acids upregulated the enzymatic activities of GST and ALDH and induced the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nfe2l2; Nrf2), a master regulator of antioxidant and detoxifying systems. These results suggest that iso-α-acid intake prevents acetaldehyde-induced liver injury by reducing oxidative stress via Nrf2-mediated gene expression. Public Library of Science 2021-02-05 /pmc/articles/PMC7864453/ /pubmed/33544749 http://dx.doi.org/10.1371/journal.pone.0246327 Text en © 2021 Takase et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Takase, Takahito
Toyoda, Tsudoi
Kobayashi, Naoyuki
Inoue, Takashi
Ishijima, Tomoko
Abe, Keiko
Kinoshita, Hiroshi
Tsuchiya, Youichi
Okada, Shinji
Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression
title Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression
title_full Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression
title_fullStr Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression
title_full_unstemmed Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression
title_short Dietary iso-α-acids prevent acetaldehyde-induced liver injury through Nrf2-mediated gene expression
title_sort dietary iso-α-acids prevent acetaldehyde-induced liver injury through nrf2-mediated gene expression
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7864453/
https://www.ncbi.nlm.nih.gov/pubmed/33544749
http://dx.doi.org/10.1371/journal.pone.0246327
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