[Abstract] Objective To investigate the protective mechanisms of Ulinastatin and dexamethasone on acute lung injury induced by Lipopolysaccharide endotoxin in rats .Methods 24 male Sprague—Dawley rats were randomly divided into four groups with 6 mice each group: control group (Con group), lipopolysaccharide group (LPS group), lipopolysaccharide plus Ulinastatin group (UTI group), lipopolysaccharide plus dexamethasone group ( DXM group). Rats were killed at 8h time points, and the protein and mRNA expression of GR in the lung were detected by western-blot and Real Time fluorescent PCR. The levels of TNF-α and IL-10 were also tested by ELISA and at the same time we would test the lung wet/dry weight radio. The pathology of lung tissue was evaluated by HE staining .Results. The protein expression levels of GR ：Compared with control group, the protein expression level of GR in LPS group was significantly lower. The protein expression levels of GR in UTI group and DXM group were higher than those in LPS group and significantly lower than those in control group .No significant differences were found between UTI and DXM group in the protein expression levels of GR；The expression levels of GRmRNA ：Compared with control group, the expression level of GRmRNA in LPS group was significantly lower, but the expression level of GRmRNA in UTI group was slightly higher than those in LPS group. No significant differences were found between UTI and LPS group in the expression levels of GRmRNA ,but the expression level of GRmRNA in DXM group was significantly higher than those in UTI group ,LPS group and Con group ；The expression level of TNF-α：Compared with control group, the expression level of TNF-αin LPS group was significantly higher, the expression level of TNF-α in UTI group and DXM group fell in between control group and LPS group, but the expression level of TNF-αin DXM group were lower than those in UTI group and higher than those in LPS group、Con group；The expression levels of IL-10：Compared with control group, the expression level of IL-10 in LPS group was significantly higher. In UTI group , the expression level of IL-10 was higher than those in LPS group. The expression level of IL-10 in DXM group fell in between control group and LPS group；The lung wet/dry weight radio：Compared with control group, the lung wet/dry weight radio in LPS group was significantly higher, the lung wet/dry weight radio in UTI group and DXM group fell in between control group and LPS group, but the lung wet/dry weight radio in DXM group were lower than those in UTI group；Lung hispathology ：necrotic abscission cells increased in alveolar space，inflammatory cells infiltration and lung interstitial edema appeared in LPS group. However，pathological changes in UTI group mad DXM group were milder than those in LPS group , pathological changes in group DXM was milder than those in UTI group.Conclusions The protective mechanisms of Ulinastatin and dexamethasone on acute lung injury induced by Lipopolysaccharide endotoxin in rats were not the same, the protective effect of dexamethasone on acute lung injury was better than Ulinastatin.