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The lipoxins are the first proresolution mediators to be recognized and described as the endogenous “braking signals” for inflammation. We evaluated the anti-inflammatory and proresolution bioactions of lipoxin A 4  in our lipopolysaccharide (LPS-)induced lung injury model. We demonstrated that lipoxin A 4  significantly improved histology of rat lungs and inhibited IL-6 and TNF-  α   in LPS-induced lung injury. In addition, lipoxin A 4  increased alveolar fluid clearance (AFC) and the effect of lipoxin A 4  on AFC was abolished by CFTR inh-172  (a specific inhibitor of CFTR). Moreover, lipoxin A 4  could increase cystic fibrosis transmembrane conductance regulator (CFTR) protein expression  in vitro  and  in vivo . In rat primary alveolar type II (ATII) cells, LPS decreased CFTR protein expression via activation of PI3K/Akt, and lipoxin A 4  suppressed LPS-stimulated phosphorylation of Akt. These results showed that lipoxin A 4  enhanced CFTR protein expression and increased AFC via PI3K/Akt pathway. Thus, lipoxin A 4  may provide a potential therapeutic approach for acute lung injury.

Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A4via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury

Contribution of CFTR to Alveolar Fluid Clearance by Lipoxin A₄via PI3K/Akt Pathway in LPS-Induced Acute Lung Injury