• Ruixue Xia, Na Fang, Yanjie Yang, Feng Xu, Lingge Zhang, and Shaoping Ji.
• Department of Respiratory and Critical Care Medicine, Henan University Huaihe Hospital, Kaifeng, China.
• Minerva Med. 2023 Oct 1; 114 (5): 652657652-657.

BackgroundThe aim of this study was to uncover the ability of PM2.5 exposure to induce apoptosis in alveolar epithelial cells by stimulating excessive production of reactive oxygen species (ROS), thus activating p38 to result in emphysema in mice.MethodsMale BALB/c mice with 6-8-week-old were exposed to 200 TPM mg/L PM2.5 for 12 weeks. Lung tissues of mice were harvested after sacrifice. Hematoxylin and eosin staining was conducted for observing alveolar structure change. Protein levels of p-p38 and p38, as well as ROS level in mouse liver tissues were determined. A549 cells were exposed to different doses of PM2.5, followed by ROS detection, protein level detection of p-p38 and p38, and apoptosis determination. After transfection of si-p38, protein level of clv-caspase3 and apoptotic rate in PM2.5-exposed A549 cells were assessed.ResultsAfter 12-week exposure to PM2.5, enlarged alveolar space, elevated ROS level in lung tissues and activated p38 were observed in mice. In PM2.5-exposed A549 cells, ROS level, p-p38 expression and apoptotic rate were dose-dependently enhanced. The antioxidant NAC reversed the above changes in PM2.5-exposed A549 cells. Silence of p38 reversed the enhanced clv-claspase3 level and apoptotic rate in PM2.5-exposed A549 cells.ConclusionsPM2.5 exposure elevates ROS level in lung tissues, and activates p38, thus leading to apoptosis of alveolar epithelial cells. PM2.5 finally results in the development of emphysema in mice.

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