Urinary trypsin inhibitor attenuates lipopolysaccharide-induced acute lung injury by blocking the activation of p38 mitogen-activated protein kinase |
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Authors: | Xinying Zhang Fengqin Liu Haiyan Liu Hongxia Cheng Wei Wang Qiang Wen Yulin Wang |
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Institution: | 1. Department of Pediatrics, Provincial Hospital Affiliated to Shandong University, 324 Jingwuweiqi Road, Jinan, 250021, China 2. Department of Pathology, Provincial Hospital Affiliated to Shandong University, Jinan, China 3. Department of Clinical Medicine, Weifang Medical College, Weifang, China
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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)-?? 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-?? 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-?? expression may be related to the inhibitory effect of UTI on p38 MAPK activation. |
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