Objective To establish paraquat(PQ)induced acute lung injury models induced by paraquat (PQ), and to study the protective effects of angiotension converting enzyme inhibitors (ACEI) with eaptopril (CAP) on the PQ posioning. Method All experiments were made in the central laboratory of Union Hospital. Human umbilical vein endothelial cells (HUVECs) were incubated with different concentration of paraquat and captopril to establish experimental models. Half of cell survival rate detected with MTF assay to judge whether the model was successful or not. Three groups were divided according to the different drug. application: normal control group without any drug intervetion, PQ group exposed to paraqnat with the concentration of 400 μmol/L and CAP group additionally exposed to captopril with concentration of 10 μmoL/L, which was repartifioned to three groups (CAPA, CAPB and CAPC) according to the different intervention time. The supematant was collected to measure the concentration of malondialdehyde(MDA) and superoxide dismutase(SOD) after PQ injury for 24 hours, cy-tochrome C detected by immunocytochemistry and apoptosis detected by flow cytometry. Data were expressed as mean±standard error of the mean (x±s). Statistical 'analysis was carried out with the soft SPSS 16.0. Results MTr assay detected the concentration & time of PQ intervention and the data of CAP groups, using the single-re-season variance analysis, F value were 56.734,172.025, P < 0.01 respectively, thus to suecessfidly construct the PQ model and determine the concentration of CAP intervention groups. Relative to the PQ group, MDA as well as levels of cytochrome C of the CAP group were significantly decreased (t = 5.913,3.945,-3.426, P <0.01); while SOD were markedly increased (t = 5.463,-2.292,-1.297, P < 0.01). It also showed that captopril markedly decreased PQ induced the rate of HUVECs apoptosis, the percentagen of PQ group apoptosis was 46.1%, while CAP groups apoptnsis were 4.3 %, 9.2% and 17 % respectively. Conclusions Captopril has the ability to scavenge reactive oxygen species, and to protect against the paraquat induced lung toxicity on HUVECs, which pro-vide the infonnafion for basic research and clinical treatment of PQ posioning. Key words: Paraquat; Captopril; Lunginjury; Angiotension converting enzyme inhibitors (ACEI) ; Hydrnsul-fide; HUNECs; Apoptosis; Poisoning