Abstract: Objective To investigate the effect of interference with Rho-associated coil formingprotein kinase 1 on lung injury induced by lipopolysaccharide (LPS) in mice. Methods C57BL / 6mice were divided into 4 groups: healthy control group, model group, negative control group and ROCK1 interference group, 10 mice each group. Acute lung injury was induced with LPS (5 mg / kg, i. p. ). The expression level of ROCK1 was detected by RT-PCR and Western blotting. The pulmonary function detection system was used to detect the airway resistance, resting ventilation and lung volume in mice. HE staining was used to observe the pathological damage of lung tissues, and Masson staining was used to observe the pulmonary fibrosis. Western blotting was used to detect the protein expression levels of α-SMA, TGF-β1 and FN. TUNEL assay was used to detect the lung cellapoptosis. The levels of iNOS, IL-6 and TNF-α were detected by ELISA. Results ROCK1 washighly expressed in the model group and the lung injury was more serious when compared with thatin the healthy control group. ROCK1 interference group had lower expression level of ROCK1 (P <0. 05), and increased airway resistance, resting ventilation and lung volume when compared withthe model group (P < 0. 05). The pathological injury and degree of fibrosis in lung tissues were improved in the ROCK1 interference group, and the expression levels of α-SMA, TGF-β1 and FN proteins were significantly decreased (P< 0. 05). The number of apoptotic cells in lung tissues was significantly decreased (P< 0. 05), and the levels of iNOS, IL-6 and TNF-α in peripheral bloodwere significantly decreased in the ROCK1 interference group when compared with those in themodel group (P < 0. 05). Conclusion Interfering ROCK1 expression can improve lung function,pulmonary fibrosis, apoptosis and inflammation in LPS-induced acute lung injury mice.

Key words: ROCK1, lipopolysaccharide, acute lung injury