Comparative effects of inhaled diesel exhaust and ambient fine particles on inflammation, atherosclerosis, and vascular dysfunction.
Comparative effects of inhaled diesel exhaust and ambient fine particles on inflammation, atherosclerosis, and vascular dysfunction.
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DOI：
10.3109/08958371003728057
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发表时间：
2010-08
影响因子：
2.1
通讯作者：
Chen LC
中科院分区：
文献类型：
--
作者：
Quan C;Sun Q;Lippmann M;Chen LC
环境空气中的PM2.5(直径小于2.5μm的颗粒物)与心血管疾病有关，但影响心血管疾病的潜在机制尚不清楚。作者调查了亚慢性吸入浓缩环境PM2.5(CAPS)、全柴油废气(WDE)或柴油废气(DEGS)是否会导致动脉粥样硬化、肺和全身炎症以及血管功能障碍的加重；以及DEG与CAPS的相互作用是否会改变心血管效应。APOE−/−小鼠同时吸入五种不同的暴露环境5小时/天，4天/周，最长5个月：(1)过滤空气(FA)；(2)CAPS(105μg/m~3)；(3)湿空气(DEP=436μg/m~3)；(4)DEG(相当于WDE组的气体水平)；(5)CAPS+DEG(PM2.5：113μg/m~3；DEG相当于WDE组)。3个月和5个月后，分析肺灌洗液和血清，并通过超声成像、苏木精-伊红(H&E染色)和EnFace苏丹IV染色对动脉粥样硬化斑块进行定量。暴露5个月后对血管功能进行评估。作者发现：(1)亚慢性吸入CAPS、WDE和DEG可增加血清血管细胞黏附分子(VCAM)-1水平并增强苯肾上腺素(PE)诱导的血管收缩；(2)对于斑块恶化，CAPS>；WDE>；DEG=FA，因此PM成分(在WDE中不存在)是斑块形成的责任；(3)动脉粥样硬化可以通过炎症和血管功能障碍以外的机械途径加剧；以及(4)尽管CAPS和DEG之间在斑块恶化方面没有显著的相互作用，但尚不清楚DEG联合暴露是否增强了CAPS对血管舒缩功能障碍和肺/系统性炎症的影响。
Ambient air PM2.5 (particulate matter less than 2.5 μm in diameter) has been associated with cardiovascular diseases (CVDs), but the underlying mechanisms affecting CVDs are unknown. The authors investigated whether subchronic inhalation of concentrated ambient PM2.5 (CAPs), whole diesel exhaust (WDE), or diesel exhaust gases (DEGs) led to exacerbation of atherosclerosis, pulmonary and systemic inflammation, and vascular dysfunction; and whether DEG interactions with CAPs alter cardiovascular effects. ApoE−/− mice were simultaneously exposed via inhalation for 5 hours/day, 4 days/week, for up to 5 months to one of five different exposure atmospheres: (1) filtered air (FA); (2) CAPs (105 μg/m3); (3) WDE (DEP = 436 μg/m3); (4) DEG (equivalent to gas levels in WDE group); and (5) CAPs+DEG (PM2.5: 113 μg/m3; with DEG equivalent to WDE group). After 3 and 5 months, lung lavage fluid and blood sera were analyzed, and atherosclerotic plaques were quantified by ultrasound imaging, hematoxylin and eosin (H&E stain), and en face Sudan IV stain. Vascular functions were assessed after 5 months of exposure. The authors showed that (1) subchronic CAPs, WDE, and DEG inhalations increased serum vascular cell adhesion molecule (VCAM)-1 levels and enhanced phenylephrine (PE)-induced vasoconstriction; (2) for plaque exacerbation, CAPs > WDE > DEG = FA, thus PM components (not present in WDE) were responsible for plaque development; (3) atherosclerosis can exacerbated through mechanistic pathways other than inflammation and vascular dysfunction; and (4) although there were no significant interactions between CAPs and DEG on plaque exacerbation, it is less clear whether the effects of CAPs on vasomotor dysfunction and pulmonary/systemic inflammation were enhanced by the DEG coexposure.
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影响因子：
2.1
作者：
Ishihara, Y;Kagawa, J
通讯作者：
Kagawa, J
影响因子：
3.8
作者：
Campen, Matthew J.;Lund, Amie K.;McDonald, Jacob D.
通讯作者：
McDonald, Jacob D.
影响因子：
24.3
作者：
Devlin, RB;Ghio, AJ;Cascio, W
通讯作者：
Cascio, W
影响因子：
11.4
作者：
Geller, VD;Sardar, SB;Sioutas, C
通讯作者：
Sioutas, C
影响因子：
10.4
作者：
Frampton MW;Stewart JC;Oberdörster G;Morrow PE;Chalupa D;Pietropaoli AP;Frasier LM;Speers DM;Cox C;Huang LS;Utell MJ
通讯作者：
Utell MJ