Abstract： Objective To investigate the molecular mechanism of PM2.5-induced injury of human aortic endothelial cells(HAECs).Methods HAECs were exposed to the collected atmospheric PM2.5 for 24 hours.Cell viability was detected by MTT assay.Interleukin-1β and 18(IL-1β and IL-18)levels were measured by Enzyme-linked immunosorbent assay(ELISA).Penthiobarbital method was used to measure the content of malondialdehyde(MDA),and the colorimetric method was used to measure the activity of lactate dehydrogenase(LDH).Western Blot and quantitative polymerase chain reaction(Q-PCR)were used to detect the expression levels of Nucleotide-binding oligomerization domain NOD-like receptor containing pyrin domain 3(NLRP3),caspase-1,IL-1β,Bax and Bcl-2.The flow cytometry and DAPI staining were performed to detect the cell apoptosis.Reactive oxygen species(ROS)and mitochondrial ROS(mtROS)levels were detected by commercial ROS and mtROS kits,respectively.The above indicators were re-examined after transfection of NLRP3 siRNA and treatment of ROS and mtROS specific inhibitors(NAC and Mito-TEMPO).Results PM2.5 exposure increased the IL-1β and IL-18 secretion in HAECs cells,increased release of MDA and LDH,and promoted cell apoptosis in a dose-dependent manner.Moreover,PM2.5 exposure significantly upregulated caspase-1 and IL-1β in HAECs,and increased ROS and mtROS levels.Transfection of NLRP3 siRNA or treatment of ROS and mtROS inhibitors could significantly inhibit the above effects.Conclusion PM2.5 activates NLRP3 inflammasomes by inducing oxidative stress in HAECs cells,thereby further inducing cell inflammation and cell apoptosis.