| Autor: |
Odashima, Masaru, Otaka, Michiro, Jin, Mario, Komatsu, Koga, Wada, Isao, Matsuhashi, Tamotsu, Horikawa, Youhei, Hatakeyama, Natsumi, Oyake, Jinko, Ohba, Reina, Linden, Joel, Watanabe, Sumio |
| Předmět: |
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| Zdroj: |
Journal of Gastroenterology; May2005, Vol. 40 Issue 5, p526-529, 4p |
| Abstrakt: |
Background. D-Galactosamine (GalN)/lipopolysaccharide (LPS)-induced liver injury is an experimental model of fulminant hepatic failure in which tumor necrosis factor-α (TNF-α) plays a pivotal role. We examined the effects of a highly selective adenosine A2A receptor agonist (ATL-146e) on GalN/LPS-induced fulminant hepatic failure. Methods. Mice were given an intraperitoneal dose of GalN (800 mg/g body weight)/LPS (100 ng/g body weight) with and without ATL-146e (0.01 μg/kg) treatment. Liver injury was assessed biochemically and histologically. Also, TNF-α levels in the serum were determined. Results. The serum liver enzyme (ALT) level in vehicle-treated mice was 20960 ± 2800 IU/ml and was reduced by 63% to 7800 ± 1670 IU/ml by treatment with 0.01 μg/kg per minute ATL146e, P < 0.05. Treatment with ATL-146e significantly reduced serum TNF-α and greatly reduced inflammation assessed by histopathologic examination compared with control mice treated with GalN/LPS. ATL-146e also reduced lethality at 12 h from 65% to 13%. Conclusion. The present findings suggest that the highly selective adenosine A2A receptor agonist (ATL-146e) prevents endotoxin-induced lethal liver injury by suppression of TNF-α secretion. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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