The model of acute lung injury (ALI) was established by intraperitoneal administration, but there was no time-point observation and comparison. ALI model was established by intraperitoneal injection of lipopolysaccharide (LPS) at the concentration of 10 mg ? kg-1 (10 mg LPS dissolved in 1 mL normal saline to prepare 1 mL ? kg-1 solution) in rats. The control group (CG) was intraperitoneally injected with saline of the same dose. In the LPS group, lung tissues were collected at 4, 6, 8, 12 and 24 h after administration. Then, the morphology changes, the ratio of wet-to-dry weight (W/D), the expression of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) proteins, the levels of malondialdehyde (MDA), the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH) were measured. To verify the success of the model, the degrees of lung injury via Western blot, RT-PCR, ELISA and other techniques were detected at different time points, and the severe time of the ALI model established was deterimined by intraperitoneal administration, which provided a stable model basis for the study of the pathogenesis of ALI in the future. The results showed that the lung injury occurred in LPS group. W/D and lung pathological changes at 12 and 24 h of LPS group were significantly different from those in the CG. Compared with the CG, the expression of IL-1β and TNF-α proteins and the content of MDA in lung tissues of LPS group increased and most significant difference was found at 12 and 24 h (p<0.01). Compared with the CG, the activities of SOD and GSH in LPS 12 h group decreased significantly (p<0.01). In conclusion, inflammation and oxidative damage were the main causes of the ALI in rats. Lung injury was most obvious 12 h after intraperitoneal injection of 10 mg ? kg-1 LPS.