标题：Urinary trypsin inhibitor attenuates lipopolysaccharide-induced acute lung injury by blocking the activation of p38 mitogen-activated protein kinase.
作者：Zhang X;Liu F;Liu H;Cheng H;Wang W;Wen Q;Wang Y
作者机构：[Zhang, X] Department of Pediatrics, Provincial Hospital Affiliated to Shandong University, 324 Jingwuweiqi Road, Jinan 250021, China;[ Liu, F] Depart 更多
通讯作者地址：[Wang, YL]Shandong Univ, Prov Hosp, Dept Pediat, 324 Jingwuweiqi Rd, Jinan 250021, Peoples R China.
来源：Inflammation research: Official journal of the European Histamine Research Society
关键词：Urinary trypsin inhibitor; Lipopolysaccharide; Acute lung injury; Tumor; necrosis factor-alpha; Interleukin-10; p38 Mitogen-activated protein; kinase
摘要：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)-alpha 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-alpha 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-alpha expression may be related to the inhibitory effect of UTI on p38 MAPK activation.