现代食品科技2025，Vol.41Issue(1)：1-7,7.DOI:10.13982/j.mfst.1673-9078.2025.1.1479
砷暴露通过激活ERK信号通路引起HepG2细胞脂质代谢紊乱
Lipid Metabolism Disorders in HepG2 cells Induced by Arsenic Exposure through ERK Signaling Pathway Activation
摘要
Abstract
To investigate the impact of dietary arsenic exposure on hepatic lipid metabolism and its underlying molecular mechanisms,C57BL/6 mice were chronically fed arsenic-containing chow,and an arsenic-exposed HepG2 cell model was used.Mouse liver structure was examined with transmission electron microscopy,and lipid metabolism indicators in HepG2 cells were analyzed through immunoblotting and assay kits.Results showed a significant reduction in both the number and size of lipid droplets in the livers of the arsenic-exposed group.In vitro experiments revealed decreased expression of Sterol Regulatory Element Binding Protein-1c(SREBP-1c)and Fatty Acid Synthesis(FASN)proteins in HepG2 cells exposed to arsenic concentrations ranging from 10 to 40 µmol/L(SREBP-1c:0.73,0.60,0.54,0.40;FASN:0.88,0.77,0.75,0.82).Levels of triglycerides(TG)and total cholesterol(TC)also declined(TG:0.94,0.78,0.78,0.73;TC:0.95,0.73,0.70,0.57),indicating arsenic-induced lipid metabolism disruption.Additionally,phosphorylated Extracellular Signal-Regulated Kinase(ERK)expression increased significantly following arsenic exposure(5.72,23.78,33.20,47.17),suggesting ERK pathway activation.Pre-treatment with PD98059,an ERK activation inhibitor,led to increased SREBP-1c and FASN expression in arsenic-exposed HepG2 cells(SREBP-1c:1.2;FASN:1.3),as well as elevated TG and TC levels(TG:1.2;TC:1.2).These findings provide a theoretical basis for the role of ERK signaling in arsenic-induced lipid metabolism disorders in HepG2 cells.关键词
砷/细胞外信号调节激酶/脂质代谢Key words
arsenic/extracellular signal-regulated kinase(ERK)/lipid metabolism引用本文复制引用
张文鑫,曾淑娴,田先兵,吴杰根,郭莲仙,梁一..砷暴露通过激活ERK信号通路引起HepG2细胞脂质代谢紊乱[J].现代食品科技,2025,41(1):1-7,7.基金项目
国家自然科学基金项目(81102850) （81102850）
广东省医学科研基金项目(A2022392) （A2022392）
广东医科大学专业建设项目(4SG21014G) （4SG21014G）
