Lipoxin A₄ ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

ABSTRACT:

Background

Acute respiratory distress syndrome (ARDS) is characterized by alveolar epithelial disruption. Lipoxins (LXs), as so-called "braking signals" of inflammation, are the first mediators identified to have dual anti-inflammatory and inflammatory pro-resolving properties.

Methods

In vivo, lipoxinA₄ was administrated intraperitoneally with 1 μg/per mouse after intra-tracheal LPS administration (10 mg/kg). Apoptosis, proliferation and epithelial-mesenchymal transition of AT II cells were measured by immunofluorescence. In vitro, primary human alveolar type II cells were used to model the effects of lipoxin A₄ upon proliferation, apoptosis and epithelial-mesenchymal transition.

Results

In vivo, lipoxin A₄ markedly promoted alveolar

SUBMITTER: Yang JX 

PROVIDER: S-EPMC6704532 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature