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Rats were intravenously injected with MCTR1 at a dose of 200\u00a0ng\/rat, 8\u00a0hours after administration of 14\u00a0mg\/kg LPS. The level of AFC was then determined in live rats. Primary rat ATII (Alveolar Type II) epithelial cells were also treated with MCTR1 (100\u00a0nmol\/L) in a culture medium containing LPS for 8\u00a0hours. MCTR1 treatment improved AFC (18.85\u00a0\u00b1\u00a02.07 vs 10.11\u00a0\u00b1\u00a01.08, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a0.0001) and ameliorated ALI in rats. MCTR1 also significantly promoted AFC by up\u2010regulating epithelial sodium channel (ENaC) and Na<jats:sup>+<\/jats:sup>\u2010K<jats:sup>+<\/jats:sup>\u2010adenosine triphosphatase (Na, K\u2010ATPase) expressions in vivo. MCTR1 also activated Na, K\u2010ATPase and elevated phosphorylated\u2010Akt (P\u2010Akt) by up\u2010regulating the expression of phosphorylated Nedd4\u20102 (P\u2010Nedd4\u20102) in vivo and in vitro. However, BOC\u20102 (ALX inhibitor), KH7 (cAMP inhibitor) and LY294002 (PI3K inhibitor) abrogated the improved AFC induced by MCTR1. Based on the findings of this study, MCTR1 may be a novel therapeutic approach to improve reabsorption of pulmonary oedema during ALI\/acute respiratory distress syndrome (ARDS).<\/jats:p>","DOI":"10.1111\/jcmm.15146","type":"journal-article","created":{"date-parts":[[2020,3,11]],"date-time":"2020-03-11T20:05:36Z","timestamp":1583957136000},"page":"4736-4747","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Maresin Conjugates in Tissue Regeneration 1 improves alveolar fluid clearance by up\u2010regulating alveolar ENaC, Na, K\u2010ATPase in lipopolysaccharide\u2010induced acute lung injury"],"prefix":"10.1111","volume":"24","author":[{"given":"Jun","family":"Han","sequence":"first","affiliation":[{"name":"Department of Anaesthesia and Critical Care The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University Zhejiang 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