Wan Guohui, Rajagopalan Sanjay, Sun Qinghua, Zhang Kezhong
Int J Physiol Pathophysiol Pharmacol. 2010 Mar 15;2(1):64-68.
Epidemiological studies have shown a strong link between air pollution and the increase of cardio-pulmonary mortality and morbidity. In particular, inhaled airborne particulate matter (PM) exposure is closely associated with the pathogenesis of air pollution-induced systemic diseases. In this study, we exposed C57BIV6 mice to environmentally relevant PM in fine and ultra fine ranges (diameter < 2.5 μm, PM(2.5)) using a "real-world" airborne PM exposure system. We investigated the pathophysiologic impact of PM(2.5) exposure in the animal model and in cultured primary pulmonary macrophages. We demonstrated that PM(2.5) exposure increased the production of reactive oxygen species (ROS) in blood vessels in vivo. Furthermore, in vitro PM(2.5) exposure experiment suggested that PM(2.5) could trigger oxidative stress response, reflected by an increased expression of the anti-oxidative stress enzymes superoxide dismutase-1 (SOD-1) and heme oxygenase-1(HO-1), in mouse primary macrophages. Together, the results obtained through our "real-world" PM exposure approach demonstrated the pathophysiologic effect of ambient PM(2.5) exposure on triggering oxidative stress in the specialized organ and cell type of an animal model. Our results and approach will be informative for the research in air pollution-associated physiology and pathology.
流行病学研究表明，空气污染与心肺疾病死亡率和发病率的增加之间存在紧密联系。特别是，吸入空气中的颗粒物（PM）暴露与空气污染诱发的全身性疾病的发病机制密切相关。在本研究中，我们使用“真实环境”空气颗粒物暴露系统，将C57BIV6小鼠暴露于环境相关的细颗粒物和超细颗粒物（直径<2.5μm，PM2.5）中。我们研究了PM2.5暴露在动物模型和原代培养肺巨噬细胞中的病理生理影响。我们证明，PM2.5暴露会增加体内血管中活性氧（ROS）的产生。此外，体外PM2.5暴露实验表明，PM2.5可触发氧化应激反应，这在小鼠原代巨噬细胞中表现为抗氧化应激酶超氧化物歧化酶-1（SOD-1）和血红素加氧酶-1（HO-1）表达增加。总之，通过我们的“真实环境”PM暴露方法获得的结果证明了环境PM2.5暴露对动物模型特定器官和细胞类型触发氧化应激的病理生理作用。我们的结果和方法将为空气污染相关生理学和病理学的研究提供信息。
