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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Acknowledgments
The authors thank the teachers from the research center in Provincial Hospital Affiliated to Shandong University for their technical assistance. We thank Prof. Aihua Ma and Dr. Wei Hao for their careful and critical reading of our first draft.
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Responsible editor: Michael Parnham.
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Zhang, X., Liu, F., Liu, H. et al. Urinary trypsin inhibitor attenuates lipopolysaccharide-induced acute lung injury by blocking the activation of p38 mitogen-activated protein kinase. Inflamm. Res. 60, 569–575 (2011). https://doi.org/10.1007/s00011-010-0305-2
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DOI: https://doi.org/10.1007/s00011-010-0305-2