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

Abstract 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 ex...

Full description

Bibliographic Details
Main Authors: Lixia Hong, Yide Xu, Dongdong Wang, Qi Zhang, Xiaoting Li, Chunfeng Xie, Jieshu Wu, Caiyun Zhong, Jinyan Fu, Shanshan Geng
Format: Article
Language:English
Published: Nature Portfolio 2023-01-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-023-28395-5
_version_ 1828056914240471040
author Lixia Hong
Yide Xu
Dongdong Wang
Qi Zhang
Xiaoting Li
Chunfeng Xie
Jieshu Wu
Caiyun Zhong
Jinyan Fu
Shanshan Geng
author_facet Lixia Hong
Yide Xu
Dongdong Wang
Qi Zhang
Xiaoting Li
Chunfeng Xie
Jieshu Wu
Caiyun Zhong
Jinyan Fu
Shanshan Geng
author_sort Lixia Hong
collection DOAJ
description Abstract 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.
first_indexed 2024-04-10T21:02:56Z
format Article
id doaj.art-3a25dac5f4414f29bbd7114a38622193
institution Directory Open Access Journal
issn 2045-2322
language English
last_indexed 2024-04-10T21:02:56Z
publishDate 2023-01-01
publisher Nature Portfolio
record_format Article
series Scientific Reports
spelling doaj.art-3a25dac5f4414f29bbd7114a386221932023-01-22T12:11:28ZengNature PortfolioScientific Reports2045-23222023-01-0113111010.1038/s41598-023-28395-5Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stressLixia Hong0Yide Xu1Dongdong Wang2Qi Zhang3Xiaoting Li4Chunfeng Xie5Jieshu Wu6Caiyun Zhong7Jinyan Fu8Shanshan Geng9Department of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityDepartment of Nutrition, Wuxi Maternal and Child Health Care HospitalDepartment of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical UniversityAbstract 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.https://doi.org/10.1038/s41598-023-28395-5
spellingShingle Lixia Hong
Yide Xu
Dongdong Wang
Qi Zhang
Xiaoting Li
Chunfeng Xie
Jieshu Wu
Caiyun Zhong
Jinyan Fu
Shanshan Geng
Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress
Scientific Reports
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
url https://doi.org/10.1038/s41598-023-28395-5
work_keys_str_mv AT lixiahong sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT yidexu sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT dongdongwang sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT qizhang sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT xiaotingli sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT chunfengxie sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT jieshuwu sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT caiyunzhong sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT jinyanfu sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress
AT shanshangeng sulforaphaneamelioratesbisphenolainducedhepaticlipidaccumulationbyinhibitingendoplasmicreticulumstress