Epidemiological studies have confirmed that PM2.5 could contribute to the development of atherosclerosis accompanied with lipids dysregulation. However, the lipids biomarkers involved in this progress remain largely unknown. In this study, a targeted lipidomic approach was used to find out the possible lipid biomarkers involved in the development of atherosclerosis after PM2.5 exposure or during a recovery period. Also, we assessed the pro-atherosclerosis effects of PM2.5 and follow-up influence using pulse wave (PW) Doppler ultrasound, oil red O staining and H&E staining. The vascular stiffness was elevated after 2-month PM2.5 exposure and might persist after 1-month recovery. While the lesions mostly concentrated in the aortic arch was significantly increased in 2-month PM2.5 exposure group and remained an increasing trend after 1-month recovery. The expressions of pro-inflammatory cytokines detected by Mouse Inflammation Array were elevated after ApoE-/- mice treated with PM2.5 for 2-month and restored following 1-month recovery. Yet, IL-10 was significantly decreased during 1-month recovery. Additionally, the targeted lipidomic analysis demonstrated that cholesterol ester (CE), phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelin (SM) were significantly increased while lysophosphatidylethanolamine (LPE), lysophosphatidylcholine (LPC), diacylglycerol (DG), triacylglycerol (TG) were reduced after 2-month PM2.5 exposure, indicating that PM2.5 could disrupt glycerophospholipids, glycerolipids and sphingolipids metabolism. And a persistent impact of PM2.5 on glycerophospholipids and glycerolipids metabolism was found after 1-month recovery. Our study demonstrated that PM2.5-induced inflammation response might promote atherosclerotic lesions probably through lipid dysregulation, and the influence probably persisted after 1-month recovery.

中文翻译：

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根据靶向脂质组学分析，PM2.5诱导的炎症和脂质组改变与动脉粥样硬化的发展有关。

流行病学研究证实，PM2.5可能会导致动脉粥样硬化的发展并伴有脂质异常。但是，参与该过程的脂质生物标志物仍是未知之数。在这项研究中，有针对性的脂质组学方法被用来找出参与PM2.5暴露后或恢复期间可能与动脉粥样硬化发展有关的脂质生物标志物。此外，我们使用脉搏波（PW）多普勒超声，油红O染色和H＆E染色评估了PM2.5对动脉粥样硬化的作用和后续影响。在暴露2个月的PM2.5后，血管僵硬度升高，并且在恢复1个月后可能会持续。虽然病变主要集中在主动脉弓，但在2个月的PM2中明显增加。5个接触组并在1个月恢复后仍保持上升趋势。小鼠炎症阵列检测到的促炎细胞因子的表达在用PM2.5处理2个月的ApoE-/-小鼠后升高，并在恢复1个月后恢复。然而，IL-10在1个月的恢复过程中显着降低。此外，靶向脂质组学分析表明，胆固醇酯（CE），磷脂酰胆碱（PC），磷脂酰乙醇胺（PE），鞘磷脂（SM）显着增加，而溶血磷脂酰乙醇胺（LPE），溶血磷脂酰胆碱（LPC），二酰基甘油（DG），三酰基甘油（在暴露2个月后暴露于PM2.5中，表明PM2.5可以破坏甘油磷脂，甘油脂和鞘脂的代谢。并持续影响PM2。5个月后发现甘油磷脂和甘油脂质代谢恢复1个月。我们的研究表明，PM2.5诱导的炎症反应可能通过脂质失调来促进动脉粥样硬化病变，并且这种影响可能在恢复1个月后仍然存在。