Acteoside inhibits apoptosis in D-Galactosamine and lipopolysaccharide- induced liver injury

Quanbo Xiong, Koji Hase, Yasuhiro Tezuka, Tsuneo Namba, Shigetoshi Kadota

Research output: Contribution to journalArticle

102 Citations (Scopus)

Abstract

We assessed the effect of acteoside, a naturally occurring antioxidative phenylethanoid, on hepatic apoptosis and the subsequent liver failure induced by D-Galactosamine (D-GalN) and lipopolysaccharide (LPS). A co-administration of D-GalN (700 mg/kg) and LPS (35 μg/kg) to mice evoked typical hepatic apoptosis characterized by DNA fragmentation and apoptotic body formation, resulting in fulminant hepatitis and lethality of mice. Pre-administration of acteoside at 10 or 50 mg/kg subcutaneously at 12 and 1 h prior to D-GalN/LPS intoxication significantly inhibited hepatic apoptosis, hepatitis and lethality. Tumor necrosis factor-α (TNF-α) secreted from LPS-stimulated macrophages is an important mediator of apoptosis in this model. Acteoside showed no apparent effect on the marked elevation of serum TNF-α, but it partially prevented in vitro TNF-α (100 ng/ml)-induced cell death in D-GalN (0.5 mM)-sensitized hepatocytes at the concentrations of 50, 100 and 200 μM. These results indicated that D-GalN/LPS-induced hepatic apoptosis can be blocked by an exogenous antioxidant, suggesting the involvement of reactive oxygen intermediates (ROIs) in TNF-α-dependent hepatic apoptosis.

Original languageEnglish
Pages (from-to)421-430
Number of pages10
JournalLife Sciences
Volume65
Issue number4
DOIs
Publication statusPublished - 1999 Jun 18
Externally publishedYes

Keywords

  • Acteoside
  • Apoptosis
  • D-galactosamine
  • Lipopolysaccharide
  • Necrosis
  • Reactive oxygen intermediates
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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