Document Detail

Urinary trypsin inhibitor attenuates hepatic ischemia-reperfusion injury by reducing nuclear factor-kappa B activation.
MedLine Citation:
PMID:  19208516     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappaB) 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<0.05). Compared with the control group, the UTI treatment groups showed significantly lower serum alanine aminotransferase and aspartate aminotransferase levels, decreased myeloperoxidase activity, and reduced NF-kappaB activation. Also downregulated was the expression of tumor necrosis factor-alpha, cytokine-induced neutrophil chemoattractant, and macrophage inflammatory protein-2 at the mRNA level. P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated. In addition, the treatment group 1 showed a better protective effect against I/R injury than the treatment group 2. CONCLUSIONS: UTI reduces NF-kappaB activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury. The protective role of UTI is more effective in prevention than in treatment.
Yi-Jun Wu; Qi Ling; Xin-Hui Zhou; Yan Wang; Hai-Yang Xie; Ji-Ren Yu; Shu-Sen Zheng
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Hepatobiliary & pancreatic diseases international : HBPD INT     Volume:  8     ISSN:  1499-3872     ISO Abbreviation:  HBPD INT     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-02-11     Completed Date:  2009-05-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101151457     Medline TA:  Hepatobiliary Pancreat Dis Int     Country:  China    
Other Details:
Languages:  eng     Pagination:  53-8     Citation Subset:  IM    
Department of General Surgery, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
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MeSH Terms
Acute-Phase Reaction / immunology
Alanine Transaminase / blood
Aspartate Aminotransferases / blood
Chemokine CXCL1 / genetics,  metabolism
Chemokine CXCL2 / genetics,  metabolism
Disease Models, Animal
Down-Regulation / drug effects,  immunology
E-Selectin / genetics,  metabolism
Glycoproteins / metabolism*,  pharmacology*
Intercellular Adhesion Molecule-1 / genetics,  metabolism
Liver Diseases / drug therapy*,  immunology,  metabolism
Mice, Inbred BALB C
NF-kappa B / metabolism*
Neutrophils / immunology
P-Selectin / genetics,  metabolism
Peroxidase / metabolism
RNA, Messenger / metabolism
Reperfusion Injury / drug therapy*,  immunology,  metabolism
Tumor Necrosis Factor-alpha / genetics,  metabolism
Reg. No./Substance:
0/Chemokine CXCL1; 0/Chemokine CXCL2; 0/Cxcl1 protein, mouse; 0/Cxcl2 protein, mouse; 0/E-Selectin; 0/Glycoproteins; 0/NF-kappa B; 0/P-Selectin; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; 126547-89-5/Intercellular Adhesion Molecule-1; 80449-32-7/urinastatin; EC; EC Aminotransferases; EC Transaminase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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