Methyl tertiary-butyl ether inhibits THP-1 macrophage cholesterol efflux in vitro and accelerates atherosclerosis in ApoE-deficient mice in vivo
甲基第三级丁基的醚在 vitro 禁止 THP-1 巨噬细胞胆固醇流出并且在 vivo 在 ApoE 缺乏的老鼠加速动脉粥样硬化作者机构:State Key Laboratory of Environmental Chemistry and Eco-ToxicologyResearch Center for Eco-Environmental SciencesChinese Academy of SciencesBeijing 100085China College of Resources and EnvironmentUniversity of Chinese Academy of SciencesBeijing 100049China School of Environmental Science and EngineeringSouthern University of Science and TechnologyShenzhen 518055China
出 版 物:《Journal of Environmental Sciences》 (环境科学学报(英文版))
年 卷 期:2021年第33卷第3期
页 面:236-247页
核心收录:
学科分类:083002[工学-环境工程] 0830[工学-环境科学与工程(可授工学、理学、农学学位)] 07[理学] 08[工学] 09[农学] 0903[农学-农业资源与环境] 0713[理学-生态学]
基 金:supported by the National Key R&D Program of China(Nos.2019YFC1605800,2018YFC0406302) the National Natural Science Foundation of China(Nos.21806179,21672255) the Strategic Priority Research Program of the Chinese Academy of Sciences(No.XDB14040201)
主 题:Methyl tertiary–butyl ether(MTBE) macrophage cholesterol efflux ApoE^(-/-)mouse Atherosclerosis
摘 要:The biosafety of methyl tertiary-butyl ether(MTBE),mainly used as a gasoline additive,has long been a contentious *** addition to its routine toxicities,MTBE has been demonstrated to disrupt glucose and lipid metabolism and contribute to the development of type2 diabetes as well as *** one of the morbidities related to dyslipidemia,atherosclerosis is worthy of being investigated under MTBE *** foam cells derived from macrophages play pivotal roles during atherosclerosis development,we studied the effects of MTBE on macrophages in vitro and assessed the effect of MTBE on atherosclerosis plaque formation with the ApoE^(-/-)mouse model in uiuo for the first *** results demonstrated that exposure to MTBE at environmentally relevant concentrations decreased the expression of ABCA1 and ABCG1,which are responsible for macrophage cholesterol efflux,at both mRNA and protein levels in THP-1 ***,treatment with MTBE inhibited the transport of cholesterol from macrophages to High-density ***^(-/-)mice exposed to MTBE at environmentally relevant concentrations(100,1000μg/kg)displayed significant increases in lesion area in the aorta and aortic root compared to vehicletreated *** analysis indicated that MTBE exposure enhanced the macrophagespecific marker Mac-2 contents within plaques in the aortic root,implying that MTBE could promote macrophage-derived foam cell formation and thus accelerate atherosclerosis plaque *** for the first time demonstrated the pro-atherogenic effect of MTBE via eliciting disruption of macrophage cholesterol efflux and accelerating foam cell formation and atherosclerosis plaque development.