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Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice

Perfluorooctanoic acid (PFOA) can accumulate in the livers of humans and animals via the food chain, resulting into liver injury, which is closely related to intestinal flora dysbiosis. Gastrodin has been reported to have hepatoprotective effect. However, whether gastrodin can alleviate PFOA-induced...

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Autores principales: Ma, Shumin, Sun, Yanyan, Zheng, Xueting, Yang, Yang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8810172/
https://www.ncbi.nlm.nih.gov/pubmed/34866532
http://dx.doi.org/10.1080/21655979.2021.2009966
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author Ma, Shumin
Sun, Yanyan
Zheng, Xueting
Yang, Yang
author_facet Ma, Shumin
Sun, Yanyan
Zheng, Xueting
Yang, Yang
author_sort Ma, Shumin
collection PubMed
description Perfluorooctanoic acid (PFOA) can accumulate in the livers of humans and animals via the food chain, resulting into liver injury, which is closely related to intestinal flora dysbiosis. Gastrodin has been reported to have hepatoprotective effect. However, whether gastrodin can alleviate PFOA-induced liver injury via modulating gut microbiota remains unclear. Herein, a PFOA-induced liver injury model was established by gavage of PFOA (5 mg/kg body weight) in 2% Tween 80 solution once daily for 6 weeks in mice, and then gastrodin in saline (20 mg/kg body weight) was used once daily for 8 weeks to treat liver damage. The biochemical indexes associated with liver function, oxidative stress, and inflammatory factors were examined. Hematoxylin-eosin staining was used to determine the liver histopathological changes. Besides, 16S rRNA sequencing was used to analyze the difference of gut microbiota between the model and treatment groups. The results showed that gastrodin significantly improved the oxidative stress caused by PFOA. Intestinal flora analysis showed that gastrodin treatment significantly increased the relative abundance of probiotics, such as Lactobacillus, Bifidobacterium, and Bacteroides, while the harmful bacteria, including Desulfovibrio were decreased. Gastrodin treatment also significantly increased the level of short-chain fatty acids (SCFAs), such as butyric acid and isobutyric acid. Spearman correlation analysis showed that the composition changes of gut microbiota and SCFAs increase were both beneficial to alleviate the liver injury caused by PFOA. To sum up, gastrodin can effectively alleviate PFOA-induced liver injury through regulating gut microbiota composition.
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spelling pubmed-88101722022-02-03 Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice Ma, Shumin Sun, Yanyan Zheng, Xueting Yang, Yang Bioengineered Research Paper Perfluorooctanoic acid (PFOA) can accumulate in the livers of humans and animals via the food chain, resulting into liver injury, which is closely related to intestinal flora dysbiosis. Gastrodin has been reported to have hepatoprotective effect. However, whether gastrodin can alleviate PFOA-induced liver injury via modulating gut microbiota remains unclear. Herein, a PFOA-induced liver injury model was established by gavage of PFOA (5 mg/kg body weight) in 2% Tween 80 solution once daily for 6 weeks in mice, and then gastrodin in saline (20 mg/kg body weight) was used once daily for 8 weeks to treat liver damage. The biochemical indexes associated with liver function, oxidative stress, and inflammatory factors were examined. Hematoxylin-eosin staining was used to determine the liver histopathological changes. Besides, 16S rRNA sequencing was used to analyze the difference of gut microbiota between the model and treatment groups. The results showed that gastrodin significantly improved the oxidative stress caused by PFOA. Intestinal flora analysis showed that gastrodin treatment significantly increased the relative abundance of probiotics, such as Lactobacillus, Bifidobacterium, and Bacteroides, while the harmful bacteria, including Desulfovibrio were decreased. Gastrodin treatment also significantly increased the level of short-chain fatty acids (SCFAs), such as butyric acid and isobutyric acid. Spearman correlation analysis showed that the composition changes of gut microbiota and SCFAs increase were both beneficial to alleviate the liver injury caused by PFOA. To sum up, gastrodin can effectively alleviate PFOA-induced liver injury through regulating gut microbiota composition. Taylor & Francis 2021-12-04 /pmc/articles/PMC8810172/ /pubmed/34866532 http://dx.doi.org/10.1080/21655979.2021.2009966 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://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/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Ma, Shumin
Sun, Yanyan
Zheng, Xueting
Yang, Yang
Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice
title Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice
title_full Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice
title_fullStr Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice
title_full_unstemmed Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice
title_short Gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice
title_sort gastrodin attenuates perfluorooctanoic acid-induced liver injury by regulating gut microbiota composition in mice
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8810172/
https://www.ncbi.nlm.nih.gov/pubmed/34866532
http://dx.doi.org/10.1080/21655979.2021.2009966
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