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 TUNEL 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 by PM2.5 at concentration of 100 μg/mL or more for 24 and 48 h. With the increase of PM2.5 concentration, the cells apoptotic rate significantly increased, the protein ex-pression of LC3Ⅱwas increased as well as the P-AKT was decreased; and the protein expression of LC3Ⅱwas in-creased significantly after AKT inhibitor treatment. Moreover, rapamycin decreased PM2.5-induced cell apoptosis, and 3-MA can promote PM2.5-induced cell apoptosis. Conclusions In H441 cells, PM2.5 activates autophagy by inhibiting activation of AKT pathway, and cell autophagy can mitigate PM2.5-induced apoptosis.