Abstract

Background and aims: Long-term of oxygen exposure can result in acute lung injury and lung fibrosis in late time. Aims: To investigate the Rho kinase inhibitor fasudil (FAS) in neonatal rats with hyperoxia-induced lung fibrosis. Methods: According to the random number tables, twenty-four Sprague-Dawley neonatal rats were randomly divided into 4 groups: Air+NS (normal saline) group, Air+FAS group, Hyperoxia+NS group and Hyperoxia+FAS group.After 21d, the subjects were sacrificed. The changes of lung histomorphology were observed; Hydroxyproline in the lung was detected by sample hydrolysis method; α-smooth muscle actin (α-SMA) protein expression in the lung was determined by immunohistochemistry method and Western-blot. Results: Pathological examination showed structural disorder and obvious fibrosis in lung tissue of Hyperoxia+NS group, and the sings of improvement in lung tissue of Hyperoxia+FAS group at 21d.The content of hydroxyproline and the α-SMA protein expression in lung tissue were both increased markedly at 21d of Hyperoxia+NS group and Hyperoxia+FAS group compared with the air groups, they were significantly reduced at 21d of Hyperoxia+FAS group compared with Hyperoxia+NS group. Conclusions: Rho kinase inhibitor fasudil could have obvious therapeutic effects on hyperoxia-induced lung fibrosis.It probably improve lung fibrosis via the inhibition of myofibroblast.

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