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Inflammation Research

Published 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

Authors: Xinying Zhang, Fengqin Liu, Haiyan Liu, Hongxia Cheng, Wei Wang, Qiang Wen, Yulin Wang

Published in: Inflammation Research | Issue 6/2011

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.

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Title: Urinary trypsin inhibitor attenuates lipopolysaccharide-induced acute lung injury by blocking the activation of p38 mitogen-activated protein kinase
Authors: Xinying Zhang
Fengqin Liu
Haiyan Liu
Hongxia Cheng
Wei Wang
Qiang Wen
Yulin Wang
Publication date: 01-06-2011
Publisher: SP Birkhäuser Verlag Basel
Published in: Inflammation Research / Issue 6/2011
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI: https://doi.org/10.1007/s00011-010-0305-2

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Abstract

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