2. Academic Validation
  3. Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress

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

  • Sci Rep. 2023 Jan 20;13(1):1147. doi: 10.1038/s41598-023-28395-5.
Lixia Hong 1,  Yide Xu 1,  Dongdong Wang 1,  Qi Zhang 1,  Xiaoting Li 1,  Chunfeng Xie 1,  Jieshu Wu 1,  Caiyun Zhong 2,  Jinyan Fu 3,  Shanshan Geng 4
Affiliations

Affiliations

  • 1 Department of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, 211166, China.
  • 2 Department of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, 211166, China. [email protected].
  • 3 Department of Nutrition, Wuxi Maternal and Child Health Care Hospital, Wuxi, 214002, Jiangsu, China. [email protected].
  • 4 Department of Nutrition and Food Safety, Center for Global Health, School of Public Health, Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing, 211166, China. [email protected].
PMID: 36670177 DOI: 10.1038/s41598-023-28395-5
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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