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.
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.
Authors: D Yoshinari; I Takeyoshi; Y Koibuchi; K Matsumoto; Y Kawashima; T Koyama; S Ohwada; Y Morishita Journal: Crit Care Med Date: 2001-03 Impact factor: 7.598
Authors: Y Kitamura; S Hashimoto; N Mizuta; A Kobayashi; K Kooguchi; I Fujiwara; H Nakajima Journal: Am J Respir Crit Care Med Date: 2001-03 Impact factor: 21.405
Authors: Michael A Matthay; Guy A Zimmerman; Charles Esmon; Jahar Bhattacharya; Barry Coller; Claire M Doerschuk; Joanna Floros; Michael A Gimbrone; Eric Hoffman; Rolf D Hubmayr; Mark Leppert; Sadis Matalon; Robert Munford; Polly Parsons; Arthur S Slutsky; Kevin J Tracey; Peter Ward; Dorothy B Gail; Andrea L Harabin Journal: Am J Respir Crit Care Med Date: 2003-04-01 Impact factor: 21.405
Authors: Dilip R Karnad; Rakesh Bhadade; Pradeep K Verma; Nivedita D Moulick; Mradul K Daga; Neelima D Chafekar; Shivakumar Iyer Journal: Intensive Care Med Date: 2014-04-16 Impact factor: 17.440