Abstract: AimTo study the protective action of ulinastatin against lipopolysaccharide (LPS)-induced acute lung injury in mice and the mechanism of its action. MethodsMice were intraperitoneally injected with ulinastatin (50 and 100 ku·kg^-1) or saline at a period of 12 h, separately, 30 min after the last injection of ulinastatin, except normal control, all mice of other groups were injected a dose of LPS 15 mg·kg^-1 via tail vein. The levels of TNFα in serum and lung were measured by ELISA. The expression of TNFα mRNA and iNOS mRNA in lung was assayed by RT-PCR. The expression of c-Fos and c-Jun protein in lung was measured by Western blotting method. And the NO₂-/NO₃- level in serum and MDA in lung were measured with kits. ResultsThe levels of NO₂^-/NO₃^- and TNFα in serum, MDA and TNFα in lung all increased after iv injection of LPS. The expressions of TNFα mRNA, iNOS mRNA, c-Fos and c-Jun in lung of LPS-injected mice were enhanced. Pretreatment with ulinastatin 100 ku·kg^-1 decreased the levels of NO₂^- / NO₃^- in serum and lung, reduced the index of lung, and inhibited the expressions of iNOS mRNA and c-Jun in lung induced by LPS in mice, while ulinastatin showed no effect on TNFα level in serum and lung. ConclusionUlinastatin protected mice from acute lung injury induced by lipopolysaccharides via inhibiting the activation of c-Jun and iNOS mRNA expression.