Wan Qiang, Cui Xiaobing, Shao Jiman, Zhou Fenghua, Jia Yuhua, Sun Xuegang, Zhao Xiaoshan, Chen Yuyao, Diao Jianxin, Zhang Lei
School of Traditional Chinese Medicine, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China.
Cell Stress Chaperones. 2014 Sep;19(5):715-24. doi: 10.1007/s12192-014-0499-2. Epub 2014 Feb 13.
Ambient particulate matter (PM) exposure has been associated with atherosclerosis. However, research on the effect of real-world exposure to ambient PM in regulating visfatin expression in an animal model is very limited. The objective is to investigate whether Beijing ambient PM exposure could accelerate atherosclerosis in ApoE knockout (ApoE(-/-)) mice by upregulating visfatin expression. Forty male ApoE(-/-) mice were exposed to untreated ambient air (PM group, n = 20) or filtered air (FA group, n = 20), 24 h/day, 7 days/week, for 2 months. During the exposure, the mass concentrations of PM2.5 and PM10 in the two groups were continuously monitored. Moreover, a receptor source apportionment model was applied to apportion sources of PM2.5. At the end of the exposure, visfatin in plasma and aorta, biomarkers of inflammation, oxidative stress and lipid metabolism in blood samples, and bronchoalveolar lavage fluid (BALF) were determined, and the plaque area of the atherosclerosis lesions was quantified. PM-exposed mice were significantly higher than FA-exposed mice in terms of plasma visfatin, OxLDL, MDA, serum TC, LDL, TNF-α as well as IL-6, TNF-α, OxLDL, and MDA in BALF, while SOD and GSH-Px activities in plasma and BALF were reduced in PM-exposed mice. Pathological analysis of the aorta demonstrated that the plaque area and visfatin protein in the PM group increased significantly compared to the FA group. Our findings indicate that ambient PM exposure could accelerate atherosclerosis, which is related to visfatin upregulation, as well as the activation of inflammation and oxidative stress.
暴露于环境颗粒物（PM）已被证实与动脉粥样硬化有关。然而，关于在动物模型中实际暴露于环境PM对内脏脂肪素表达调节作用的研究非常有限。本研究旨在探讨北京环境PM暴露是否会通过上调内脏脂肪素表达加速载脂蛋白E基因敲除（ApoE(-/-)）小鼠的动脉粥样硬化进程。将40只雄性ApoE(-/-)小鼠每天24小时、每周7天分别暴露于未处理的环境空气（PM组，n = 20）或过滤空气（FA组，n = 20）中，持续2个月。在暴露期间，持续监测两组中PM2.5和PM10的质量浓度。此外，应用受体源解析模型对PM2.5的来源进行解析。暴露结束时，测定血浆和主动脉中的内脏脂肪素、血液样本中炎症、氧化应激和脂质代谢的生物标志物以及支气管肺泡灌洗液（BALF），并对动脉粥样硬化病变的斑块面积进行量化。与FA组相比，PM暴露组小鼠血浆中的内脏脂肪素、氧化型低密度脂蛋白（OxLDL）、丙二醛（MDA）、血清总胆固醇（TC）、低密度脂蛋白（LDL）、肿瘤坏死因子-α（TNF-α）以及BALF中的白细胞介素-6（IL-6）、TNF-α、OxLDL和MDA显著升高，而PM暴露组小鼠血浆和BALF中的超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）活性降低。主动脉的病理分析表明，与FA组相比，PM组的斑块面积和内脏脂肪素蛋白显著增加。我们的研究结果表明，环境PM暴露可加速动脉粥样硬化，这与内脏脂肪素上调以及炎症和氧化应激的激活有关。
