Title: Fasudil Alleviates LPS-induced Lung Injury by Resorting Aqua-porin 5 Expression and Inhibiting Inflammation in Lung


Authors: Jingjing Wang , Hui Kong , Jian Xu, Yanli Wang, Hong Wang, Weiping Xie


Institution: Department of Respiratory & Critical Care Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, PR China.


Abstract: Fasudil, a selective rho kinase (ROCK) inhibitor, has been reported to play a beneficial role in systemic inflammation/lung injury, but its mechanism for ameliorating pulmonary edema and inflammation remains unclear. In the present study, by using hematoxylin-and-eosin (HE) staining, immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), quantitative real time PCR (qRT-PCR) and western blotting, we showed that fasudil attenuated LPS-induced lung pathological injury, decreased lung edema, and suppressed inflammatory responses including leukocytes infiltration and IL-6 production. Further, fasudil upregulated LPS-induced AQP5 reduction and inhibited NF-kB activation in the lungs of mice. Our results suggest that fasudil could restore the expression of AQP5 to eliminate LPS-induced lung edema and prevent LPS-induced pulmonary inflammation by inhibiting the inflammatory pathway. Collectively, blockade of ROCK pathway by fasudil may be a potential strategy for acute lung injury.


Keywords: acute lung injury, Aquaporin 5, fasudil, fliud transport, NF-kB


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J Biomed Res published on 20 June, 2017, doi:10.7555/JBR.31.20170024