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Mechanism of relieving hyperoxia-induced lung fibrosis of neonatal rats by Rock inhibitor fasudil

QI Xiu-jie1,2, LI Jing2, XU Feng2, FANG Fang2   

  1. 1.Ministry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Training Base of Clinical Resident Standard Training in Chongqing, Children's Hospital of Chongqing Medical University, Chongqing 400014, China; 2.Department of Pediatric Intensive Care Unit, Children's Hospital of Chongqing Medical University, Chongqing 400014, China
  • Online:2014-10-28 Published:2014-10-28
  • Supported by:

    National Natural Science Foundation of China, 81101442

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Abstract:

Objective To investigate the mechanism of relieving hyperoxia-induced lung fibrosis of neonatal rats by the Rho kinase (Rock) inhibitor fasudil (FAS). Methods According to the random number tables, 24 Sprague-Dawley neonatal rats were randomly divided into the air group (control group), FAS air group, hyperoxia group, and FAS hyperoxia group. Animal models of each group were established. Rats were sacrificed after models were established for 21d. The radial alveolar count (RAC) was conducted for lung tissue. Expressions of transforming growth factor-β1 (TGF-β1) protein and Rock1 and myosin phosphatase target subunit-1 phosphorylation (p-MYPT1) proteins in Rho/Rock signaling pathway were detected by the Western blotting. Results Compared to the air group, the RAC of the hyperoxia group decreased significantly (P<0.05). The RAC of the FAS hyperoxia group increased compared to the hyperoxia group, but the difference was not statistically significant (P>0.05). Compared to the air group, the expression of TGF-β1 protein in pulmonary tissues of the hyperoxia group up-regulated significantly (P<0.05), while the expression of TGF-β1 protein in pulmonary tissues of the FAS hyperoxia group down-regulated significantly compared to the hyperoxia group (P<0.05). Compared to the air group, the expression of Rock1 protein in pulmonary tissues of the hyperoxia group tended to up-regulate, but the difference was not statistically significant (P>0.05), while the expression of p-MYPT1 protein up-regulated significantly (P<0.05). Compared to the hyperoxia group, the expression of Rock1 protein in pulmonary tissues of the FAS hyperoxia group down-regulated, but the difference was not statistically significant (P>0.05), while the expression of p-MYPT1 protein down-regulated significantly (P<0.05). Conclusion FAS can relieve hyperoxia-induced lung fibrosis of neonatal rats to a certain extent by downregulating the expression of TGF-β1. The regulation mechanism may be relevant to inhibiting the activation of Rho/Rock signaling pathway.

Key words: hyperoxia, lung fibrosis, fasudil, transforming growth factor-β1, Rho/Rock signaling pathway