Platelet-activating factor is a mediator in tumor necrosis factor/galactosamine-induced lethality

J Inflamm. 1995;46(3):139-43.

Abstract

We here report that administration to mice of WEB2170, a potent platelet-activating factor (PAF) receptor antagonist, prevents both PAF-induced and murine tumor necrosis factor (TNF)-induced lethality in galactosamine (GalN)-sensitized mice. Furthermore, we demonstrate that pretreatment with alpha 1-acid glycoprotein (AGP) or interleukin-1 (IL-1) protects against TNF-induced, but not against PAF-induced lethality. We conclude that PAF is a mediator in TNF/GalN-induced lethal shock, but that the protection conferred by AGP or IL-1 pretreatment is not at the level of scavenging PAF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Azepines / pharmacology*
  • Female
  • Galactosamine / pharmacology*
  • Interleukin-1 / pharmacology
  • Mice
  • Mice, Inbred C57BL
  • Orosomucoid / pharmacology
  • Platelet Activating Factor / antagonists & inhibitors
  • Platelet Activating Factor / physiology*
  • Platelet Activating Factor / toxicity
  • Platelet Aggregation Inhibitors / pharmacology*
  • Shock / physiopathology
  • Triazoles / pharmacology*
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / physiology
  • Tumor Necrosis Factor-alpha / toxicity*

Substances

  • Azepines
  • Interleukin-1
  • Orosomucoid
  • Platelet Activating Factor
  • Platelet Aggregation Inhibitors
  • Triazoles
  • Tumor Necrosis Factor-alpha
  • Galactosamine
  • bepafant