Erschienen in:
01.06.2011 | Original Research Paper
Urinary trypsin inhibitor attenuates lipopolysaccharide-induced acute lung injury by blocking the activation of p38 mitogen-activated protein kinase
verfasst von:
Xinying Zhang, Fengqin Liu, Haiyan Liu, Hongxia Cheng, Wei Wang, Qiang Wen, Yulin Wang
Erschienen in:
Inflammation Research
|
Ausgabe 6/2011
Einloggen, um Zugang zu erhalten
Abstract
Objective
To investigate the protective effect of urinary trypsin inhibitor (UTI) in a rat model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the underlying molecular mechanism.
Methods
Rats were randomly assigned into three groups: control group, LPS treatment group and LPS/UTI treatment group. The serum concentrations of tumor necrosis factor (TNF)-α and interleukin (IL)-10 were measured by ELISA. The expression of p38 mitogen-activated protein kinase (MAPK) in lung tissues was determined by Western blot analysis.
Results
Administration of UTI reduced the lung wet/dry weight ratio and ameliorated the tissue damage. In the LPS/UTI treatment group, levels of TNF-α were significantly lower than those in the LPS treatment group, while the levels of IL-10 were significantly higher than those in the LPS treatment group. Western blot analysis revealed that UTI inhibited the phosphorylation of p38 MAPK in lung tissues.
Conclusions
UTI attenuates LPS-induced ALI, probably by adjusting the balance between proinflammatory and anti-inflammatory cytokines. The mechanism responsible for the decreased TNF-α expression may be related to the inhibitory effect of UTI on p38 MAPK activation.