RESUMO
PM2.5, as one of the most harmful pollutant in the atmospheric environment and population health, has received much attention. We monitored PM2.5 levels at five sampling sites in the Lanzhou City and collected PM2.5 particles from two representative sites for cytotoxicity experiment. The cytotoxicity of PM2.5 samples on A549 cells and migration ability of the cells were respectively detected by Cell Counting kit-8 (CCK-8) assay and scratch assay. We detected the levels of cellular inflammatory factors and oxidative damage-related biochemical indexes. RT-qPCR was used to detect the mRNA levels of NF-κB and epithelial-mesenchymal transition (EMT)-related genes. We found that the Lanlian Hotel station had the highest PM2.5 annual average concentration. The annual average concentration change curve of PM2.5 showed a roughly "U"-shaped distribution during the whole sampling period. The cytotoxicity experiment showed the viability of A549 cells decreased and the scratch healing rate increased in the 200 and 400 µg/mL PM2.5-treated groups. We also found 400 µg/mL PM2.5 induced changes in the mRNA levels of NF-κB and EMT-related genes, the mRNA levels of IKK-α, NIK, and NF-κB in the 400 µg/mL PM2.5 group were higher than those in the control group. The mRNA levels of E-cadherin decreased and α-SMA increased in the 400 µg/mL PM2.5 groups, and the mRNA levels of Fibronectin increased in the 400 µg/mL PM2.5 groups. Moreover, we found hydroxyl radical scavenging ability and T-AOC levels were lower, and LPO levels were higher in the 200 and 400 µg/mL PM2.5 groups, and the SOD activity of cells in the 400 µg/mL PM2.5 group decreased. And compared with the control group, the levels of TNF-α were higher in the 200 and 400 µg/mL PM2.5 groups and the levels of IL-1 were higher in the 400 µg/mL PM2.5 group. The results indicated that the cytotoxicity of atmospheric PM2.5 was related to oxidative damage, inflammatory response, NF-κB activity and EMT.