Open AccessLipoxin A4 ameliorates alveolar fluid clearance disturbance in lipopolysaccharide-induced lung injury via aquaporin 5 and MAPK signaling pathway
Author(s) -
Fang Ba,
Xiaoming Zhou,
Yingqi Zhang,
Cen Wu,
Shaochun Xu,
Li-qin Wu,
Jiayang Li,
Yan Yin,
Xia Gu
Publication year - 2019
Publication title -
journal of thoracic disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.682
H-Index - 60
eISSN - 2077-6624
pISSN - 2072-1439
DOI - 10.21037/jtd.2019.08.86
Subject(s) - bronchoalveolar lavage , inflammation , medicine , lipopolysaccharide , lung , cytokine , pulmonary edema , p38 mitogen activated protein kinases , pharmacology , tumor necrosis factor alpha , mapk/erk pathway , immunology , signal transduction , microbiology and biotechnology , biology
A characteristic of acute lung injury (ALI) is the inflammatory damage of alveolar fluid transport. Lipoxins are endogenous lipids involving in the resolution of inflammation. It is found that lipoxin A4 (LXA4) has the distinct properties to improve the anti-edema and pro-resolution function in inflammation. Since aquaporins (AQPs) have essential roles in the integrity of barrier function during fluid transport, especially AQP5 in the maintaining of the epithelium permeability, the current study is aimed to evaluate the potential role of LXA4 in regulating alveolar fluid clearance (AFC) during fluid transport and the corresponding change of AQP5 in the lung.