Objective   To investigate the effects of dexamethasone and fasudil on oleic acid-induced acute lung injury in mice and the roles of Rho-associated coiled-coil forming kinase (ROCK) in this process.    Methods   Totally 140 SPF grade C57 mice were randomly and equally divided into 4 groups: normal control

acute lung injury group

dexamethasone group and fasudil group. The animals of the later 3 groups were inflicted by an injection of 0.6 mg/g oleic acid through tail vein to induce acute lung injury model

and then followed by injecting normal saline at same volume

5 mg/kg dexamethasone and 10 mg/kg fasudil respectively. The normal control group only received normal saline injection. All mice were sacrificed 24 h after injury and the lungs were resected. The pulmonary pathology was examined by HE staining

the activities of ROCK1 and ROCK2 were assayed by ELISA

the expression levels of ROCK1 and ROCK1 protein were detected by Western blot analysis

and the expression level of IL-β mRNA were observed by real-time PCR.    Results   After treatment with dexamethasone or fasudil

the bleeding and infiltration in lung tissue induced by oleic acid were attenuated

the lung water content was decreased significantly

the activities of ROCK1 and ROCK2 were inhibited

and the expression level of IL-1β mRNA was declined. Dexamethasone had no effect on the expression level of ROCK1 but upregulated the expression of ROCK2 significantly. Both of the expression level of ROCK1 and ROCK2 had no significant changes after treatment with fasudil.    Conclusion   Both of dexamethasone and fasudil attenuate the lung injury induced by oleic acid through inhibiting the activity of ROCK. The different effects of dexamethasone and fasudil on the expression levels of ROCK1 and ROCK2 suggest that effects of ROCK1 and ROCK2 in the treatment of dexamethasone or fasudil in oleic acid induced lung injury are different.