期刊
ENVIRONMENT INTERNATIONAL
卷 136, 期 -, 页码 -出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.envint.2019.105444
关键词
PM2.5; Atherosclerosis; Inflammation; Lipidomic; Glycerophospholipids; Glycerolipids
资金
- National Key R&D Program of China [2017YFC0211600, 2017YFC0211602, 2017YFC0211606]
- National Natural Science Foundation of China [81571130090, 81673204]
- Beijing Nova Program [Z181100006218027]
- Young Elite Scientists Sponsorship Program of China Association for Science and Technology [2017QNRC001]
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 0 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 PM(2.5)induced inflammation response might promote atherosclerotic lesions probably through lipid dysregulation, and the influence probably persisted after 1-month recovery.
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