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双酚 F 和双酚 S 促进人脂肪干细胞中的脂质积累和脂肪生成。

Bisphenol F and bisphenol S promote lipid accumulation and adipogenesis in human adipose-derived stem cells.

机构信息

University of Granada, Centre for Biomedical Research, E-18016, Granada, Spain; Department of Radiology and Physical Medicine, School of Medicine, University of Granada, E-18071, Granada, Spain; Instituto de Investigación Biosanitaria (ibs.GRANADA), E-18012, Granada, Spain.

University of Granada, Centre for Biomedical Research, E-18016, Granada, Spain; Department of Radiology and Physical Medicine, School of Medicine, University of Granada, E-18071, Granada, Spain.

出版信息

Food Chem Toxicol. 2021 Jun;152:112216. doi: 10.1016/j.fct.2021.112216. Epub 2021 Apr 15.

Abstract

Bisphenol F (BPF) and bisphenol S (BPS) are increasingly used as substitutes for bisphenol A (BPA), an endocrine disrupting chemical (EDC) with obesogenic activity. We investigated the in vitro effects of BPS and BPF on the adipogenesis of human adipose-derived stem cells (hASCs) exposed to different doses (0.01, 0.1, 1, 10 and 25 μM), stopping the adipogenic process at 7 or 14 days. Intracellular lipid accumulation was quantified by the Oil Red O assay, gene expression of peroxisome proliferator-activated receptor gamma (PPARγ), CCAT/enhancer-binding protein (C/EBPα), lipoprotein-lipase (LPL) and fatty acid binding protein 4 (FABP4), by quantitative real-time polymerase chain reaction (qRT-PCR) and protein levels by Western Blot. hASCs with BPF or BPS produced a linear dose-response increase in intracellular lipid accumulation and in gene expression of the adipogenic markers, confirmed by protein levels. Co-treatment ICI 182,780 significantly inhibited BPF- but not BPS-induced lipid accumulation. Given the affinity of bisphenols for diverse nuclear receptors, their obesogenic effects may result from a combination of pathways rather than a single mechanism. Further research is warranted on the manner in which chemicals interfere with adipogenic differentiation. To our best knowledge, this report shows for the first time the obesogenic potential of BPF in hASCs.

摘要

双酚 F(BPF)和双酚 S(BPS)越来越多地被用作双酚 A(BPA)的替代品,BPA 是一种具有肥胖作用的内分泌干扰化学物质(EDC)。我们研究了 BPS 和 BPF 在不同剂量(0.01、0.1、1、10 和 25 μM)下对人脂肪来源干细胞(hASC)脂肪生成的体外影响,在 7 或 14 天停止脂肪生成过程。通过油红 O 测定法定量测定细胞内脂质积累,通过定量实时聚合酶链反应(qRT-PCR)测定过氧化物酶体增殖物激活受体 γ(PPARγ)、CCAAT/增强子结合蛋白(C/EBPα)、脂蛋白脂肪酶(LPL)和脂肪酸结合蛋白 4(FABP4)的基因表达,并通过 Western Blot 测定蛋白水平。BPF 或 BPS 处理的 hASC 产生细胞内脂质积累和脂肪生成标志物基因表达的线性剂量反应增加,这通过蛋白水平得到证实。ICI 182,780 的共同处理显著抑制了 BPF 但不抑制 BPS 诱导的脂质积累。鉴于双酚类物质与多种核受体的亲和力,其肥胖作用可能是多种途径而不是单一机制的结果。需要进一步研究化学物质干扰脂肪生成分化的方式。据我们所知,本报告首次显示了 BPF 在 hASC 中的肥胖潜力。

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