Polydatin protects against lipopolysaccharide-induced fulminant hepatic failure in D-galactosamine-sensitized mice.
Int J Immunopathol Pharmacol
; 25(4): 923-34, 2012.
Article
em En
| MEDLINE
| ID: mdl-23298483
ABSTRACT
Fulminant hepatic failure (FHF) is a devastating clinical syndrome with extremely poor prognosis and high mortality. Therefore, better treatment is urgently needed. Polydatin (PD), a traditional anti-inflammatory drug, has been described to protect against liver injury induced by certain hepatotoxins. The present study investigated the protective effect of PD against lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced FHF in mice and the underlying mechanism. Mice were pretreated with an increasing dose of PD (10, 30, and 100 mg/kg), following LPS/D-GalN challenge. The liver injury was assessed biochemically and histologically. We found that PD exerted a protective effect on LPS/D-GalN-induced FHF as evidenced by reducing sera alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, diminishing liver histopathological injury, and lowering mortality in a dose-dependent manner. In addition, pretreatment mice with PD dose-dependently suppressed tumor necrosis factor-alpha (TNF-alpha) production, myeloperoxidase (MPO) activity, intercellular adhesion molecule-1 (ICAM-1) and endothelial cell adhesion molecule-1 (ECAM-1) expression, caspase-3 activation, and transcription factor nuclear factor-kappa B(NF-kB) activity induced by LPS. These results suggested that PD could effectively protect from LPS/D-GalN-induced FHF and the protective effect afforded by PD probably contributed to reduce TNF-alpha production via inhibiting NF-kB activation.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Estilbenos
/
Lipopolissacarídeos
/
Falência Hepática Aguda
/
Galactosamina
/
Glucosídeos
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Int J Immunopathol Pharmacol
Assunto da revista:
ALERGIA E IMUNOLOGIA
/
FARMACOLOGIA
/
PATOLOGIA
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
China