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Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis

The gut–liver axis has emerged as a key player in the progression of non-alcoholic fatty liver disease (NAFLD). Sulforaphane (SFN) is a bioactive compound found in cruciferous vegetables; however, it has not been reported whether SFN improves NAFLD via the gut–liver axis. C57BL/6 mice were fed a hig...

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Autores principales: Xu, Ye, Huang, Xianghui, Huangfu, Bingxin, Hu, Yanzhou, Xu, Jia, Gao, Ruxin, Huang, Kunlun, He, Xiaoyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9920698/
https://www.ncbi.nlm.nih.gov/pubmed/36771448
http://dx.doi.org/10.3390/nu15030743
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author Xu, Ye
Huang, Xianghui
Huangfu, Bingxin
Hu, Yanzhou
Xu, Jia
Gao, Ruxin
Huang, Kunlun
He, Xiaoyun
author_facet Xu, Ye
Huang, Xianghui
Huangfu, Bingxin
Hu, Yanzhou
Xu, Jia
Gao, Ruxin
Huang, Kunlun
He, Xiaoyun
author_sort Xu, Ye
collection PubMed
description The gut–liver axis has emerged as a key player in the progression of non-alcoholic fatty liver disease (NAFLD). Sulforaphane (SFN) is a bioactive compound found in cruciferous vegetables; however, it has not been reported whether SFN improves NAFLD via the gut–liver axis. C57BL/6 mice were fed a high-fat and high-fructose (HFHFr) diet, with or without SFN gavage at doses of 15 and 30 mg·kg(−1) body weight for 12 weeks. The results showed that SFN reduced weight gain, hepatic inflammation, and steatosis in HFHFr mice. SFN altered the composition of gut microbes. Moreover, SFN enhanced the intestinal tight junction protein ZO-1, reduced serum LPS, and inhibited LPS/TLR4 and ERS pathways to reduce intestinal inflammation. As a result, SFN protected the intestinal integrity and declined the gut-derived LPS translocations to the liver in HFHFr diet-induced mice. SFN decreased the liver LPS levels and inhibited the LPS/TLR4 pathway activations, thus inhibiting the pro-inflammatory cytokines. Notably, Spearman correlation analysis showed that the protective effect of SFN on intestinal barrier integrity and its anti-inflammatory effect on the liver was associated with improved intestinal dysbiosis. Above all, dietary intervention with SFN attenuates NAFLD through the gut–liver axis.
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spelling pubmed-99206982023-02-12 Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis Xu, Ye Huang, Xianghui Huangfu, Bingxin Hu, Yanzhou Xu, Jia Gao, Ruxin Huang, Kunlun He, Xiaoyun Nutrients Article The gut–liver axis has emerged as a key player in the progression of non-alcoholic fatty liver disease (NAFLD). Sulforaphane (SFN) is a bioactive compound found in cruciferous vegetables; however, it has not been reported whether SFN improves NAFLD via the gut–liver axis. C57BL/6 mice were fed a high-fat and high-fructose (HFHFr) diet, with or without SFN gavage at doses of 15 and 30 mg·kg(−1) body weight for 12 weeks. The results showed that SFN reduced weight gain, hepatic inflammation, and steatosis in HFHFr mice. SFN altered the composition of gut microbes. Moreover, SFN enhanced the intestinal tight junction protein ZO-1, reduced serum LPS, and inhibited LPS/TLR4 and ERS pathways to reduce intestinal inflammation. As a result, SFN protected the intestinal integrity and declined the gut-derived LPS translocations to the liver in HFHFr diet-induced mice. SFN decreased the liver LPS levels and inhibited the LPS/TLR4 pathway activations, thus inhibiting the pro-inflammatory cytokines. Notably, Spearman correlation analysis showed that the protective effect of SFN on intestinal barrier integrity and its anti-inflammatory effect on the liver was associated with improved intestinal dysbiosis. Above all, dietary intervention with SFN attenuates NAFLD through the gut–liver axis. MDPI 2023-02-01 /pmc/articles/PMC9920698/ /pubmed/36771448 http://dx.doi.org/10.3390/nu15030743 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. 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 Article
Xu, Ye
Huang, Xianghui
Huangfu, Bingxin
Hu, Yanzhou
Xu, Jia
Gao, Ruxin
Huang, Kunlun
He, Xiaoyun
Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis
title Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis
title_full Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis
title_fullStr Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis
title_full_unstemmed Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis
title_short Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis
title_sort sulforaphane ameliorates nonalcoholic fatty liver disease induced by high-fat and high-fructose diet via lps/tlr4 in the gut–liver axis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9920698/
https://www.ncbi.nlm.nih.gov/pubmed/36771448
http://dx.doi.org/10.3390/nu15030743
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