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Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice

BACKGROUND: Alcoholic liver disease (ALD) represents a chronic wide-spectrum of liver injury caused by consistently excessive alcohol intake. Few satisfactory advances have been made in management of ALD. Thus, novel and more practical treatment options are urgently needed. Flaxseed oil (FO) is rich...

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Autores principales: Zhang, Xiaoxia, Wang, Hao, Yin, Peipei, Fan, Hang, Sun, Liwei, Liu, Yujun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5322643/
https://www.ncbi.nlm.nih.gov/pubmed/28228158
http://dx.doi.org/10.1186/s12944-017-0431-8
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author Zhang, Xiaoxia
Wang, Hao
Yin, Peipei
Fan, Hang
Sun, Liwei
Liu, Yujun
author_facet Zhang, Xiaoxia
Wang, Hao
Yin, Peipei
Fan, Hang
Sun, Liwei
Liu, Yujun
author_sort Zhang, Xiaoxia
collection PubMed
description BACKGROUND: Alcoholic liver disease (ALD) represents a chronic wide-spectrum of liver injury caused by consistently excessive alcohol intake. Few satisfactory advances have been made in management of ALD. Thus, novel and more practical treatment options are urgently needed. Flaxseed oil (FO) is rich in α-linolenic acid (ALA), a plant-derived n-3 polyunsaturated fatty acids (PUFAs). However, the impact of dietary FO on chronic alcohol consumption remains unknown. METHODS: In this study, we assessed possible effects of dietary FO on attenuation of ALD and associated mechanisms in mice. Firstly, mice were randomly allocated into four groups: pair-fed (PF) with corn oil (CO) group (PF/CO); alcohol-fed (AF) with CO group (AF/CO); PF with FO group (PF/FO); AF with FO group (AF/FO). Each group was fed modified Lieber-DeCarli liquid diets containing isocaloric maltose dextrin a control or alcohol with corn oil and flaxseed oil, respectively. After 6 weeks feeding, mice were euthanized and associated indications were investigated. RESULTS: Body weight (BW) was significantly elevated in AF/FO group compared with AF/CO group. Dietary FO reduced the abnormal elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in chronic ethanol consumption. Amelioration of these parameters as well as liver injury via HE staining in dietary FO supplementation in ALD demonstrated that dietary FO can effectively benefit for the protection against ALD. To further understand the underlying mechanisms, we investigated the inflammatory cytokine levels and gut microbiota. A series of inflammatory cytokines, including TNF-α, IL-1β, IL-6 and IL-10, were determined. As a result, TNF-α, IL-1β and IL-6 were decreased in AF/FO group compared with control group; IL-10 showed no significant alteration between AF/CO and AF/FO groups (p > 0.05). Sequencing and analysis of gut microbiota gene indicated that a reduction of Porphyromonadaceae and Parasutterella, as well as an increase in Firmicutes and Parabacteroides, were seen in AF group compared with PF control. Furthermore, dietary FO in ethanol consumption group induced a significant reduction in Proteobacteria and Porphyromonadaceae compared with AF/CO group. CONCLUSION: Dietary FO ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota, thus can potentially serve as an inexpensive interventions for the prevention and treatment of ALD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12944-017-0431-8) contains supplementary material, which is available to authorized users.
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spelling pubmed-53226432017-03-01 Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice Zhang, Xiaoxia Wang, Hao Yin, Peipei Fan, Hang Sun, Liwei Liu, Yujun Lipids Health Dis Research BACKGROUND: Alcoholic liver disease (ALD) represents a chronic wide-spectrum of liver injury caused by consistently excessive alcohol intake. Few satisfactory advances have been made in management of ALD. Thus, novel and more practical treatment options are urgently needed. Flaxseed oil (FO) is rich in α-linolenic acid (ALA), a plant-derived n-3 polyunsaturated fatty acids (PUFAs). However, the impact of dietary FO on chronic alcohol consumption remains unknown. METHODS: In this study, we assessed possible effects of dietary FO on attenuation of ALD and associated mechanisms in mice. Firstly, mice were randomly allocated into four groups: pair-fed (PF) with corn oil (CO) group (PF/CO); alcohol-fed (AF) with CO group (AF/CO); PF with FO group (PF/FO); AF with FO group (AF/FO). Each group was fed modified Lieber-DeCarli liquid diets containing isocaloric maltose dextrin a control or alcohol with corn oil and flaxseed oil, respectively. After 6 weeks feeding, mice were euthanized and associated indications were investigated. RESULTS: Body weight (BW) was significantly elevated in AF/FO group compared with AF/CO group. Dietary FO reduced the abnormal elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in chronic ethanol consumption. Amelioration of these parameters as well as liver injury via HE staining in dietary FO supplementation in ALD demonstrated that dietary FO can effectively benefit for the protection against ALD. To further understand the underlying mechanisms, we investigated the inflammatory cytokine levels and gut microbiota. A series of inflammatory cytokines, including TNF-α, IL-1β, IL-6 and IL-10, were determined. As a result, TNF-α, IL-1β and IL-6 were decreased in AF/FO group compared with control group; IL-10 showed no significant alteration between AF/CO and AF/FO groups (p > 0.05). Sequencing and analysis of gut microbiota gene indicated that a reduction of Porphyromonadaceae and Parasutterella, as well as an increase in Firmicutes and Parabacteroides, were seen in AF group compared with PF control. Furthermore, dietary FO in ethanol consumption group induced a significant reduction in Proteobacteria and Porphyromonadaceae compared with AF/CO group. CONCLUSION: Dietary FO ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota, thus can potentially serve as an inexpensive interventions for the prevention and treatment of ALD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12944-017-0431-8) contains supplementary material, which is available to authorized users. BioMed Central 2017-02-22 /pmc/articles/PMC5322643/ /pubmed/28228158 http://dx.doi.org/10.1186/s12944-017-0431-8 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Zhang, Xiaoxia
Wang, Hao
Yin, Peipei
Fan, Hang
Sun, Liwei
Liu, Yujun
Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice
title Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice
title_full Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice
title_fullStr Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice
title_full_unstemmed Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice
title_short Flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice
title_sort flaxseed oil ameliorates alcoholic liver disease via anti-inflammation and modulating gut microbiota in mice
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5322643/
https://www.ncbi.nlm.nih.gov/pubmed/28228158
http://dx.doi.org/10.1186/s12944-017-0431-8
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