Abstract | BACKGROUND AND AIMS: METHODS: ALF was induced in male Wistar rats by the intraperitoneal injection of GalN (500 mg/kg) and LPS (50 microg/kg). Immediately after GalN+LPS injection, rats were treated with intravenous injection of E5564 (3 mg/kg). The cumulative survival rates of GalN+LPS-induced ALF rats were compared between those with and without E5564 treatment. RESULTS: CONCLUSIONS: TLR4 antagonist E5564 reduced GalN+LPS-induced acute liver injury in rats and improved the overall survival rate of GalN+LPS-induced ALF rats. It may contribute to the treatment of ALF through blocking endotoxin-induced TNF-alpha overproduction of macrophages.
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Authors | Toshiyuki Kitazawa, Tatsuhiro Tsujimoto, Hideto Kawaratani, Hiroshi Fukui |
Journal | Journal of gastroenterology and hepatology
(J Gastroenterol Hepatol)
Vol. 25
Issue 5
Pg. 1009-12
(May 2010)
ISSN: 1440-1746 [Electronic] Australia |
PMID | 20546456
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Biomarkers
- E5564
- Lipid A
- Lipopolysaccharides
- Tlr4 protein, rat
- Toll-Like Receptor 4
- Tumor Necrosis Factor-alpha
- lipopolysaccharide, E coli O55-B5
- Galactosamine
- Aspartate Aminotransferases
- Alanine Transaminase
- Bilirubin
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Topics |
- Alanine Transaminase
(blood)
- Animals
- Aspartate Aminotransferases
(blood)
- Bilirubin
(blood)
- Biomarkers
(blood)
- Disease Models, Animal
- Galactosamine
- Injections, Intravenous
- Lipid A
(administration & dosage, analogs & derivatives, pharmacology)
- Lipopolysaccharides
- Liver
(drug effects, immunology, pathology)
- Liver Failure, Acute
(chemically induced, drug therapy, immunology)
- Male
- Rats
- Rats, Wistar
- Time Factors
- Toll-Like Receptor 4
(antagonists & inhibitors, metabolism)
- Tumor Necrosis Factor-alpha
(blood)
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