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Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice

This study confirmed the change in functional composition and alcohol-induced acute liver injury in Aloe arborescens after fermentation. An acute liver injury was induced by administration of ethanol (3 g/kg/day) to C57BL/6J mice for 5 days. A fermented A. arborescens Miller leaf (FAAL) extract was...

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Autores principales: Kim, Min Ju, Hurh, Joon, Kim, Ha-Rim, Lee, Sang-Wang, Sin, Hong-Sig, Kim, Sang-Jun, Noh, Eun-mi, Oh, Boung-Jun, Kim, Seon-Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society for Microbiology and Biotechnology 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10164728/
https://www.ncbi.nlm.nih.gov/pubmed/36788475
http://dx.doi.org/10.4014/jmb.2211.11044
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author Kim, Min Ju
Hurh, Joon
Kim, Ha-Rim
Lee, Sang-Wang
Sin, Hong-Sig
Kim, Sang-Jun
Noh, Eun-mi
Oh, Boung-Jun
Kim, Seon-Young
author_facet Kim, Min Ju
Hurh, Joon
Kim, Ha-Rim
Lee, Sang-Wang
Sin, Hong-Sig
Kim, Sang-Jun
Noh, Eun-mi
Oh, Boung-Jun
Kim, Seon-Young
author_sort Kim, Min Ju
collection PubMed
description This study confirmed the change in functional composition and alcohol-induced acute liver injury in Aloe arborescens after fermentation. An acute liver injury was induced by administration of ethanol (3 g/kg/day) to C57BL/6J mice for 5 days. A fermented A. arborescens Miller leaf (FAAL) extract was orally administered 30 minutes before ethanol treatment. After fermentation, the emodin content was approximately 13 times higher than that of the raw material. FAAL extract significantly attenuated ethanol-induced aspartate aminotransferase, alanine aminotransferase, and triglyceride increases in serum and liver tissue. Histological analysis revealed that FAAL extract inhibits inflammatory cell infiltration and fat accumulation in liver tissues. The cytochrome P450 2E1, superoxide dismutase, and glutathione (GSH), which involved in alcohol-induced oxidative stress, were effectively regulated by FAAL extract in serum and liver tissues, except for GSH. FAAL also maintained the antioxidant defense system by upregulating heme oxygenase 1 and nuclear factor erythroid 2-related factor 2 protein expression. In addition, FAAL extract inhibited the decrease in alcohol dehydrogenase and aldehyde dehydrogenase activity, which promoted alcohol metabolism and prevented the activation of inflammatory response. Our results suggest that FAAL could be used as a potential therapeutic agent for ethanol-induced acute liver injury.
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spelling pubmed-101647282023-05-09 Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice Kim, Min Ju Hurh, Joon Kim, Ha-Rim Lee, Sang-Wang Sin, Hong-Sig Kim, Sang-Jun Noh, Eun-mi Oh, Boung-Jun Kim, Seon-Young J Microbiol Biotechnol Research article This study confirmed the change in functional composition and alcohol-induced acute liver injury in Aloe arborescens after fermentation. An acute liver injury was induced by administration of ethanol (3 g/kg/day) to C57BL/6J mice for 5 days. A fermented A. arborescens Miller leaf (FAAL) extract was orally administered 30 minutes before ethanol treatment. After fermentation, the emodin content was approximately 13 times higher than that of the raw material. FAAL extract significantly attenuated ethanol-induced aspartate aminotransferase, alanine aminotransferase, and triglyceride increases in serum and liver tissue. Histological analysis revealed that FAAL extract inhibits inflammatory cell infiltration and fat accumulation in liver tissues. The cytochrome P450 2E1, superoxide dismutase, and glutathione (GSH), which involved in alcohol-induced oxidative stress, were effectively regulated by FAAL extract in serum and liver tissues, except for GSH. FAAL also maintained the antioxidant defense system by upregulating heme oxygenase 1 and nuclear factor erythroid 2-related factor 2 protein expression. In addition, FAAL extract inhibited the decrease in alcohol dehydrogenase and aldehyde dehydrogenase activity, which promoted alcohol metabolism and prevented the activation of inflammatory response. Our results suggest that FAAL could be used as a potential therapeutic agent for ethanol-induced acute liver injury. The Korean Society for Microbiology and Biotechnology 2023-04-28 2023-01-27 /pmc/articles/PMC10164728/ /pubmed/36788475 http://dx.doi.org/10.4014/jmb.2211.11044 Text en Copyright © 2023 by the authors. Licensee KMB https://creativecommons.org/licenses/by/4.0/This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)
spellingShingle Research article
Kim, Min Ju
Hurh, Joon
Kim, Ha-Rim
Lee, Sang-Wang
Sin, Hong-Sig
Kim, Sang-Jun
Noh, Eun-mi
Oh, Boung-Jun
Kim, Seon-Young
Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice
title Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice
title_full Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice
title_fullStr Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice
title_full_unstemmed Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice
title_short Fermented Aloe arborescens Miller Leaf Extract Suppresses Acute Alcoholic Liver Injury via Antioxidant and Anti-Inflammatory Effects in C57BL/6J Mice
title_sort fermented aloe arborescens miller leaf extract suppresses acute alcoholic liver injury via antioxidant and anti-inflammatory effects in c57bl/6j mice
topic Research article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10164728/
https://www.ncbi.nlm.nih.gov/pubmed/36788475
http://dx.doi.org/10.4014/jmb.2211.11044
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