Fasudil alleviates LPS-induced lung injury by restoring aquaporin 5 expression and inhibiting inflammation in lungs.

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-<font style="font-family:Symbol">k</font>B 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.

• Authors: Jing-Jing Wang, Hui Kong, Jian Xu, Yan-Li Wang, Hong Wang, Wei-Ping Xie
• Journal: Journal of biomedical research (J Biomed Res) Vol. 33 Issue 3 Pg. 156-163 (Jun 04 2019) ISSN: 1674-8301 [Print] China
• PMID: 28963443 (Publication Type: Journal Article)