Tobacco smoke exposure exacerbates silica-induced pulmonary toxicity in rats

Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.既往研究表明，吸烟可诱导氧化应激与炎症反应，而二者均为与矽肺（silicosis）发生发展密切相关的已知致病因素。然而，香烟烟雾暴露在矽肺发病过程中的确切作用及其潜在分子机制尚未完全阐明。为此，本研究旨在探究吸烟（若存在影响）对结晶二氧化硅（crystalline silica）诱导的肺部应答的作用及其潜在机制。本研究以雄性Fischer 344大鼠（Fischer 344 rats）为实验对象，将其分别暴露于空气、结晶二氧化硅、香烟烟雾或香烟烟雾联合结晶二氧化硅环境中，随后检测各组大鼠的肺毒性与肺部基因表达谱（gene expression profiles）。结果显示，结晶二氧化硅暴露可引发显著肺毒性，而香烟烟雾暴露会进一步加重该损伤；与对照组大鼠相比，分别暴露于香烟烟雾、结晶二氧化硅以及二者联合暴露的大鼠肺部基因表达谱均存在显著差异。