Abstract: Objective To investigate the function of autophagy in the process of PM2.5-induced apoptosis. Methods PM2.5 was obtained from Zhanjiang in 2016. Human lung adenocarcinoma cells H441 were treated with PM2.5 at different concentrations for different times. Cell proliferation was analyzed by MTT assay; Cell apoptosis was assessed by PI and Annexin V double staining and TUNNEL assay. The expression of autophagy marker LC3II, AKT and P-AKT protein was examined by Western blot (WB). H441 cells were treated with PM2.5 following treatment with rapamycin or 3-MA, Cell viability was evaluated by trypan blue staining. Results Compared with the control group, cell proliferation was significantly inhibited at 100 μg/mL or more PM2.5 treated for 24 and 48 h. With the increase of PM2.5 concentration, the cells apoptotic rate increased significantly, the protein expression of LC3II was increased as well as the P-AKT was decreased; and the protein expression of LC3II was increased significantly after AKT inhibitor treatment. Moreover, rapamycin could decrease PM2. 5-induced cell apoptosis, and 3-MA can promotes PM2.5-induced cell apoptosis. Conclusions In H441 cells, PM2.5 activates autophagy by inhibiting activation of AKT pathway, and autophagy can mitigate PM2.5-induced apoptosis.

Key words: PM2.5, Autophagy, AKT, H441