Diesel exhaust particulate increases the size and complexity of lesions in atherosclerotic mice.
Diesel exhaust particulate increases the size and complexity of lesions in atherosclerotic mice.
复制标题
DOI：
10.1186/1743-8977-10-61
复制
发表时间：
2013-12-11
影响因子：
10
通讯作者：
Hadoke PW
中科院分区：
文献类型：
--
作者：
Miller MR;McLean SG;Duffin R;Lawal AO;Araujo JA;Shaw CA;Mills NL;Donaldson K;Newby DE;Hadoke PW
柴油废气颗粒物(DEP)是城市空气污染的主要成分，与动脉粥样硬化的形成和心肌梗死的沉积有关。我们假设DEP暴露会增加和破坏载脂蛋白E缺陷(ApoE−/−)小鼠的动脉粥样硬化病变。APOE−/−小鼠被喂以“西方饮食”(8周)，以诱导“复杂的”动脉粥样硬化斑块，与正常饮食喂养的野生型小鼠进行平行实验。在喂养的最后4周内，小鼠每周两次滴注(口咽吸入)35μL DEP(1 mg/mLSRM2975)或赋形剂(生理盐水)。通过胸主动脉内膜染色和头臂动脉组织学检查来评估动脉粥样硬化负荷。−/−组小鼠头臂动脉粥样硬化斑块面积(59±10%)明显大于对照组(32±7%；P = 0.017)。此外，DEP组小鼠每段动脉有更多的斑块(2.4±0.2 vs 1.8±0.2；P = 0.048)和埋藏纤维层(1.2±0.2 vs 0.4±0.1；P = 0.028)。这些变化与肺部炎症和肝脏中抗氧化剂基因表达增加有关，但与内皮功能、血脂或全身炎症无关。动脉粥样硬化的增加是由柴油废气中的颗粒物成分导致的，它产生了具有潜在更脆弱表型的高级斑块。这些结果与去除颗粒物成分将减少柴油废气对心血管的不利影响的建议是一致的。
Diesel exhaust particulate (DEP), a major component of urban air pollution, has been linked to atherogenesis and precipitation of myocardial infarction. We hypothesized that DEP exposure would increase and destabilise atherosclerotic lesions in apolipoprotein E deficient (ApoE−/−) mice. ApoE−/− mice were fed a ‘Western diet’ (8 weeks) to induce ‘complex’ atherosclerotic plaques, with parallel experiments in normal chow fed wild-type mice. During the last 4 weeks of feeding, mice received twice weekly instillation (oropharyngeal aspiration) of 35 μL DEP (1 mg/mL, SRM-2975) or vehicle (saline). Atherosclerotic burden was assessed by en-face staining of the thoracic aorta and histological examination of the brachiocephalic artery. Brachiocephalic atherosclerotic plaques were larger in ApoE−/− mice treated with DEP (59±10%) than in controls (32±7%; P = 0.017). In addition, DEP-treated mice had more plaques per section of artery (2.4±0.2 vs 1.8±0.2; P = 0.048) and buried fibrous layers (1.2±0.2 vs 0.4±0.1; P = 0.028). These changes were associated with lung inflammation and increased antioxidant gene expression in the liver, but not with changes in endothelial function, plasma lipids or systemic inflammation. Increased atherosclerosis is caused by the particulate component of diesel exhaust producing advanced plaques with a potentially more vulnerable phenotype. These results are consistent with the suggestion that removal of the particulate component would reduce the adverse cardiovascular effects of diesel exhaust.
登录
查看更多内容
影响因子：
3.8
作者：
Campen, Matthew J.;Lund, Amie K.;McDonald, Jacob D.
通讯作者：
McDonald, Jacob D.
DOI：
10.1006/faat.1995.1022
发表时间：
1995-02-01
期刊：
FUNDAMENTAL AND APPLIED TOXICOLOGY
影响因子：
--
作者：
HENDERSON, RF;DRISCOLL, KE;BARR, EB
通讯作者：
BARR, EB
影响因子：
3.8
作者：
Driscoll, KE;Costa, DL;Schlesinger, RB
通讯作者：
Schlesinger, RB
影响因子：
8.3
作者：
Cassee FR;Campbell A;Boere AJ;McLean SG;Duffin R;Krystek P;Gosens I;Miller MR
通讯作者：
Miller MR
影响因子：
5.3
作者：
Bai N;Kido T;Suzuki H;Yang G;Kavanagh TJ;Kaufman JD;Rosenfeld ME;van Breemen C;Eeden SF
通讯作者：
Eeden SF