Title: Fasudil alleviates LPS-induced lung Injury by restoring aquaporin 5 expression and inhibiting inflammation in lungs
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, China.
Abstract: Fasudil, a selective rho kinase (ROCK) inhibitor, has been reported to play a beneficial role in systemic inflammation in acute lung injury, but its mechanism for ameliorating pulmonary edema and inflammation remains unclear. Using hematoxylin-and-eosin (H&E) staining, immunohistochemistry, enzyme-linked immunosorbent assay, quantitative real time PCR and Western blotting, we found that fasudil attenuated LPS-induced lung injury, decreased lung edema, and suppressed inflammatory responses including leukocyte infiltration and IL-6 production. Further, fasudil upregulated LPS-induced aquaporin 5 reduction and inhibited NF-kB activation in the lungs of mice. Our results suggest that fasudil could restore the expression of aquaporin 5 to eliminate LPS-induced lung edema and prevent LPS-induced pulmonary inflammation by blocking the inflammatory pathway. Collectively, blockade of the ROCK pathway by fasudil may be a potential strategy for the treatment of acute lung injury.
Keywords: acute lung injury, aquaporin 5, fasudil, fliud transport, NF-kB
Full Text: JBR-2017-0024.pdf
J Biomed Res published on 20 June, 2017, doi: 10.7555/JBR.31.20170024