Inhaled diesel emissions alter atherosclerotic plaque composition in ApoE-/- mice
Inhaled diesel emissions alter atherosclerotic plaque composition in ApoE-/- mice
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DOI：
10.1016/j.taap.2009.10.021
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发表时间：
2010-02-01
影响因子：
3.8
通讯作者：
McDonald, Jacob D.
中科院分区：
文献类型：
--
作者：
Campen, Matthew J.;Lund, Amie K.;McDonald, Jacob D.
最近的流行病学研究表明，与交通相关的空气污染可能对心血管健康产生不利影响。先前的研究表明，汽油排放可以诱导多种酶途径参与动脉粥样硬化斑块的形成和发展。作为直接比较，本研究检查了柴油发动机排放对这些途径的影响，并进一步检查了对血管病变病理学的影响。载脂蛋白 E 缺失小鼠同时接受高脂肪饮食，并暴露于四种浓度的柴油机排放物中，加上通过过滤去除颗粒 (PM) 的高浓度柴油机排放物，每天 6 小时，持续 50 天。随后检测主动脉基质金属蛋白酶 9、内皮素 1 和其他几种生物标志物的变化。柴油引起血管重塑和主动脉脂质过氧化基因标记的剂量相关变化； PM 的过滤并没有显着改变这些血管反应，表明排气中的气体部分是主要驱动因素。主动脉瓣叶切片的免疫组织化学分析显示，病变面积没有净增加，但富含脂质的区域显着减少，巨噬细胞积累和胶原蛋白含量呈增加趋势，表明柴油机尾气暴露使斑块进入更脆弱、可能更脆弱的状态。结合之前的研究，这些结果表明，移动源的全部排放可能对促进慢性血管疾病具有重要作用。 (C) 2009 Elsevier Inc. 保留所有权利。
Recent epidemiological studies suggest that traffic-related air pollution may have detrimental effects on cardiovascular health. Previous studies reveal that gasoline emissions can induce several enzyme pathways involved in the formation and development of atherosclerotic plaques. As a direct comparison, the present study examined the impact of diesel engine emissions on these pathways, and further examined the effects on vascular lesion pathology. Apolipoprotein E-null mice were simultaneously placed on a high-fat chow diet and exposed to four concentrations, plus a high concentration exposure with particulates (PM) removed by filtration, of diesel emissions for 6 h/day for 50 days. Aortas were subsequently assayed for alterations in matrix metalloproteinase-9, endothelin-1, and several other biomarkers. Diesel induced dose-related alterations in gene markers of vascular remodeling and aortic lipid peroxidation; filtration of PM did not significantly alter these vascular responses, indicating that the gaseous portion of the exhaust was a principal driver. Immunohistochemical analysis of aortic leaflet sections revealed no net increase in lesion area, but a significant decrease in lipid-rich regions and increasing trends in macrophage accumulation and collagen content, suggesting that plaques were advanced to a more fragile, potentially more vulnerable state by diesel exhaust exposure. Combined with previous studies, these results indicate that whole emissions from mobile sources may have a significant role in promoting chronic vascular disease. (C) 2009 Elsevier Inc. All rights reserved.