Objective:To investigate the protective effects of fasudil,a Rho kinase inhibitor,on the inflammation of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice secondary to sepsis and its probably mechanism in mice. Methods:C57BL/6 mice were randomly assigned to the control group,the LPS group,the LPS+fasudil (10 mg/kg) group and the LPS+dexamethasone (Dex,5 mg/kg) group. Mortality rates of different timing of each group was assessed after the establishment of the model. Mice were sacrificed at 6 h after LPS injection. Serum,bronchoalveolar lavage fluid (BALF) and lung tissues were collected. ELISA was performed to analyze the level of TNF-α,IL-1β and IL-10 in the serum,analyze the cell count and the protein content in BALF,stain with hematoxylin and eosin;test the wet-to-dry (W/D) weight;measure the content of myeloperoxidase (MPO) content in lung tissue by ELISA. Results:Fasudil significantly improved the mortality rates and prolonged the survival time of mice,relieved inflammatory injury and edema of lung tissue,and decreased MPO content. Moreover,fasudil down regulated the expression of TNF-α and IL-1β and up regulated IL-10 in serum. Conclusion:Fasudil effectively relieved LPS-induced ALI,which may be relevant to controlling the inflammatory response in the lungs.