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BACKGROUND:Urinary trypsin inhibitor (UTI) inhibits the inlfammatory response and protects against ischemia-reperfusion (I/R) injury. The inlfammatory response is mediated by nuclear factor-kappa B (NF-κB) and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines. We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS:Treatment group 1 (UTI given 5 minutes prior to liver ischemia), treatment group 2 (UTI given 5 minutes after the anhepatic phase) and a control group were investigated. Blood and liver samples were obtained and compared at 1, 3, 6 and 24 hours after reperfusion. RESULTS:Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group (P