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...
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Nature Portfolio
2023-01-01
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Series: | Scientific Reports |
Online Access: | https://doi.org/10.1038/s41598-023-28395-5 |
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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. |
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institution | Directory Open Access Journal |
issn | 2045-2322 |
language | English |
last_indexed | 2024-04-10T21:02:56Z |
publishDate | 2023-01-01 |
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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 |
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