Background PM2.5 in air pollutants can cause inflammation in airway epithelial cells, and N-acetylcysteine (NAC) can effectively reduce PM2.5-induced inflammation, but the related autophagy mechanism has been rarely studied. The study on autophagy mechanism will provide a new method for inhibiting PM2.5-induced airway inflammation.
Objective To investigate the protective effect of NAC on PM2.5-induced injury of bronchial epithelial cells.
Methods Bronchial epithelial cells (BEAS-2B) were divided into control group, PM2.5 group, PM2.5+NAC group according to different exposure factors. The control group was treated with ordinary medium for 16 hours. The PM2.5 group was pretreated with ordinary medium for 4 hours and then treated with PM2.5 medium for 12 hours. The PM2.5+NAC group was pretreated with NAC medium for 4 hours and then treated with PM2.5 medium for 12 hours. Flow cytometry was used to analyze cell apoptosis. LC3 fluorescence was observed by fluorescence confocal microscope, LC3Ⅱ/LC3Ⅰ and P62 were observed by Western Blot. The occurrence of autophagy in the three groups was analyzed.
Results Compared with control group and PM2.5+NAC group, the apoptosis of BEAS-2B cells in PM2.5 group increased significantly, while the apoptosis of BEAS-2B cells induced by PM2.5 (100 μg/mL) in PM2.5+NAC group was significantly inhibited by NAC. The immunofluorescence result showed that compared with the control group, the fluorescence of LC3 in PM2.5 group significantly increased. However, it decreased significantly in PM2.5+NAC group when compared with PM2.5 group.
Conclusion NAC can inhibit PM2.5-induced apoptosis and autophagy of human bronchial epithelial cells, thereby reducing cell damage.
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