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.
Department of Nutrition, Wuxi Maternal and Child Health Care Hospital, Wuxi, 214002, Jiangsu, China.
Sci Rep. 2023 Jan 20;13(1):1147. doi: 10.1038/s41598-023-28395-5.
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.
本研究旨在探讨内质网（ER）应激在双酚 A（BPA）诱导的肝脂质积累中的作用，以及萝卜硫素（SFN）在这一过程中的保护作用。本研究采用人肝细胞系（LO2）和 C57/BL6J 小鼠，研究 BPA 触发的肝脂质积累及其潜在机制。检测肝脂质积累、甘油三酯（TG）水平、ER 应激途径中与脂生成相关基因和蛋白的表达水平。结果表明，BPA 处理增加了脂滴数量、TG 水平和与脂生成相关基因的 mRNA 表达水平，并激活了 ER 应激途径。这些变化可被 ER 应激抑制剂 4-苯丁酸所抑制。SFN 处理可阻断 BPA 改变的肝脂质代谢，并改善 BPA 诱导的 ER 应激相关标志物。总之，这些发现表明，BPA 通过激活 ER 应激促进肝脂质积累，而 SFN 通过缓解 ER 应激逆转了这些 BPA 作用。
