Urinary trypsin inhibitor attenuates lipopolysaccharide-induced acute lung injury by blocking the activation of p38 mitogen-activated protein kinase.

Autor: Xinying Zhang, Fengqin Liu, Haiyan Liu, Hongxia Cheng, Wei Wang, Qiang Wen, Yulin Wang
Předmět:
Zdroj: Inflammation Research; Jun2011, Vol. 60 Issue 6, p569-575, 7p, 1 Color Photograph, 1 Diagram, 3 Graphs
Abstrakt: 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. [ABSTRACT FROM AUTHOR]
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