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Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress

The aim of the present study was to investigate the role of endoplasmic reticulum (ER) stress in bisphenol A (BPA) – induced hepatic lipid accumulation as well as the protective effects of Sulforaphane (SFN) in this process. Human hepatocyte cell line (LO2) and C57/BL6J mice were used to examine BPA...

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Autores principales: Hong, Lixia, Xu, Yide, Wang, Dongdong, Zhang, Qi, Li, Xiaoting, Xie, Chunfeng, Wu, Jieshu, Zhong, Caiyun, Fu, Jinyan, Geng, Shanshan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9859828/
https://www.ncbi.nlm.nih.gov/pubmed/36670177
http://dx.doi.org/10.1038/s41598-023-28395-5
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author Hong, Lixia
Xu, Yide
Wang, Dongdong
Zhang, Qi
Li, Xiaoting
Xie, Chunfeng
Wu, Jieshu
Zhong, Caiyun
Fu, Jinyan
Geng, Shanshan
author_facet Hong, Lixia
Xu, Yide
Wang, Dongdong
Zhang, Qi
Li, Xiaoting
Xie, Chunfeng
Wu, Jieshu
Zhong, Caiyun
Fu, Jinyan
Geng, Shanshan
author_sort Hong, Lixia
collection PubMed
description The aim of the present study was to investigate the role of endoplasmic reticulum (ER) stress in bisphenol A (BPA) – induced hepatic lipid accumulation as well as the protective effects of Sulforaphane (SFN) in this process. Human hepatocyte cell line (LO2) and C57/BL6J mice were used to examine BPA-triggered hepatic lipid accumulation and the underlying mechanism. Hepatic lipid accumulation, triglycerides (TGs) levels, the expression levels of lipogenesis-related genes and proteins in the ER stress pathway were measured. It was revealed that BPA treatment increased the number of lipid droplets, the levels of TG and mRNAs expression of lipogenesis-related genes, and activated the ER stress pathway. These changes were inhibited by an ER stress inhibitor 4-phenylbutyric acid. SFN treatment abrogated BPA-altered hepatic lipid metabolism and ameliorated BPA-induced ER stress-related markers. Together, these findings suggested that BPA activated ER stress to promote hepatic lipid accumulation, and that SFN reversed those BPA effects by alleviating ER stress.
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spelling pubmed-98598282023-01-22 Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress Hong, Lixia Xu, Yide Wang, Dongdong Zhang, Qi Li, Xiaoting Xie, Chunfeng Wu, Jieshu Zhong, Caiyun Fu, Jinyan Geng, Shanshan Sci Rep Article The aim of the present study was to investigate the role of endoplasmic reticulum (ER) stress in bisphenol A (BPA) – induced hepatic lipid accumulation as well as the protective effects of Sulforaphane (SFN) in this process. Human hepatocyte cell line (LO2) and C57/BL6J mice were used to examine BPA-triggered hepatic lipid accumulation and the underlying mechanism. Hepatic lipid accumulation, triglycerides (TGs) levels, the expression levels of lipogenesis-related genes and proteins in the ER stress pathway were measured. It was revealed that BPA treatment increased the number of lipid droplets, the levels of TG and mRNAs expression of lipogenesis-related genes, and activated the ER stress pathway. These changes were inhibited by an ER stress inhibitor 4-phenylbutyric acid. SFN treatment abrogated BPA-altered hepatic lipid metabolism and ameliorated BPA-induced ER stress-related markers. Together, these findings suggested that BPA activated ER stress to promote hepatic lipid accumulation, and that SFN reversed those BPA effects by alleviating ER stress. Nature Publishing Group UK 2023-01-20 /pmc/articles/PMC9859828/ /pubmed/36670177 http://dx.doi.org/10.1038/s41598-023-28395-5 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Hong, Lixia
Xu, Yide
Wang, Dongdong
Zhang, Qi
Li, Xiaoting
Xie, Chunfeng
Wu, Jieshu
Zhong, Caiyun
Fu, Jinyan
Geng, Shanshan
Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
title Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
title_full Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
title_fullStr Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
title_full_unstemmed Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
title_short Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
title_sort sulforaphane ameliorates bisphenol a-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9859828/
https://www.ncbi.nlm.nih.gov/pubmed/36670177
http://dx.doi.org/10.1038/s41598-023-28395-5
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