Cigarette-smoke-induced atherogenic lipid profiles in plasma and vascular tissue of apolipoprotein E-deficient mice are attenuated by smoking cessation
Cigarette-smoke-induced atherogenic lipid profiles in plasma and vascular tissue of apolipoprotein E-deficient mice are attenuated by smoking cessation
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DOI：
10.1016/j.atherosclerosis.2013.03.036
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发表时间：
2013-07-01
期刊：
影响因子：
5.3
通讯作者：
Peitsch, Manuel
中科院分区：
文献类型：
--
作者：
Lietz, Michael;Berges, An;Peitsch, Manuel
烟草烟雾对脂质代谢和动脉细胞功能产生干扰，加速动脉粥样硬化。脂质组学已成为帮助阐明动脉粥样硬化脂质相关机制的关键技术。在这项研究中，我们调查了戒烟对斑块发展和各种脂质分子类别和种类的主动脉弓含量的影响。将载脂蛋白E缺陷小鼠暴露于新鲜空气（假手术）或主流香烟烟雾（CS）6个月，或CS 3个月后假手术3个月（停止组）。分析血浆和主动脉弓的脂质、血浆脂蛋白谱和斑块形态测量。我们已经表明，CS暴露加速斑块大小和总胆固醇含量的主动脉弓在3个月和6个月。胆固醇酯、磷脂、鞘磷脂和鞘糖脂的相对富集显著增加。戒烟减缓斑块进展，并导致血浆和主动脉弓中许多脂质物质的水平较低。而CS暴露促进小鼠主动脉中脂质的快速积累，戒烟转化为从血管壁缓慢清除脂质。尽管戒烟依赖性代谢变化导致动物体重增加，但暴露停止后血管中致动脉粥样硬化脂质的积累停止，表明戒烟的临床益处直接转化为血管壁及其脂质组成。(C)2013作者由爱思唯尔有限公司出版。保留所有权利。
Tobacco smoke exerts perturbations on lipid metabolism and arterial cell function that accelerate atherosclerosis. Lipidomics has emerged as a key technology in helping to elucidate the lipid-related mechanisms of atherosclerosis. In this study, we investigated the effects of smoking cessation on plaque development and aortic arch content of various lipid molecular classes and species. Apolipoprotein E-deficient mice were exposed to fresh air (sham) or to mainstream cigarette smoke (CS) for 6 months, or to CS for 3 months followed by sham for 3 months (cessation group). Lipids from plasma and aortic arches, plasma lipoprotein profiles and plaque morphometry measurements were analyzed. We already showed that CS exposure accelerated plaque size and total cholesterol content of the aortic arch at 3 and 6 months. Marked increases were seen in the relative enrichment of cholesteryl esters, phospholipids, sphingomyelins, and glycosphingolipids. Smoking cessation slowed plaque progression and resulted in lower levels of many lipid species in plasma and aortic arch. While CS exposure promoted rapid lipid accumulation in mouse aorta, smoking cessation translated into a slow removal of lipids from the vessel wall. Despite the smoking cessation-dependent metabolic changes leading to increased animal body weight, accumulation of proatherogenic lipids in the vessel was halted after exposure cessation, indicating that the clinical benefits of smoking cessation translate directly to the vessel wall and its lipid makeup. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.