Laboratory of Soropidemiology and Immunobiology Laboratory, School of Medicine, University of São Paulo, Brazil.
Atherosclerosis. 2009 Dec;207(2):368-73. doi: 10.1016/j.atherosclerosis.2009.04.041. Epub 2009 May 13.
We analyzed the impact of chronic exposure to urban air pollution on the development of atherosclerosis. Hyperlipemic mice (LDLR(-/-)) were submitted to a high fat diet and air pollution for four months. We measured the susceptibility of LDL to oxidative modifications (TBARS), the presence of anti-oxLDL and an apoB-derived peptide (apoB-D) in blood and the degree of atherosclerosis in the aortic arch. Air pollution increased the susceptibility of LDL to oxidation as well as anti-oxLDL and anti-apo-B levels. These levels were even higher than in mice submitted to a high fat diet and non-polluted air. The lipid content of the atherosclerotic plaques in the aorta was increased in groups with a high cholesterol diet independently of the air quality. However, the thickness of the arterial wall was greater in mice fed a high lipid diet with polluted air. Thus, we conclude that urban air pollution exacerbates the susceptibility of LDL to oxidation, atherogenesis and vascular remodeling in hyperlipemic mice and that an immune response accompanies this process.
我们分析了慢性暴露于城市空气污染对动脉粥样硬化发展的影响。高脂饮食喂养的载脂蛋白 B 基因敲除(LDLR(-/-))小鼠(apoB(-/-))接受了为期四个月的高脂饮食和空气污染暴露。我们测量了 LDL 对氧化修饰的易感性(TBARS)、血液中抗 oxLDL 和载脂蛋白 B 衍生肽(apoB-D)的存在以及主动脉弓处动脉粥样硬化的程度。空气污染增加了 LDL 的氧化易感性以及抗 oxLDL 和抗 apo-B 水平。这些水平甚至高于高脂饮食和未受污染空气暴露的小鼠。无论空气质量如何,高胆固醇饮食组的动脉粥样硬化斑块的脂质含量均增加。然而,在高脂饮食加空气污染的小鼠中,动脉壁的厚度更大。因此,我们得出结论,城市空气污染可加剧载脂蛋白 B 基因敲除(apoB(-/-))小鼠 LDL 的氧化易感性、动脉粥样硬化形成和血管重塑,并且该过程伴随免疫反应。