Fluorofenidone protects mice from lethal endotoxemia through the inhibition of TNF-alpha and IL-1beta release

Int Immunopharmacol. 2010 May;10(5):580-3. doi: 10.1016/j.intimp.2010.02.005. Epub 2010 Feb 13.

Abstract

The pathogenesis of sepsis is mediated in part by bacterial endotoxin, which stimulates macrophages/monocytes to sequentially release proinflammatory factors like TNF-alpha and IL-1beta. Fluorofenidone (AKF-PD) is a novel pyridone agent, which exerts a strong antifibrotic effect. In this work, we showed that AKF-PD also exert an inhibitory effect on acute systemic inflammatory response. AKF-PD treatment significantly increased survival in animals with established endotoxemia. In addition, AKF-PD treatment significantly reduced circulating levels of TNF-alpha and IL-1beta during endotoxemia. In macrophage cultures, AKF-PD inhibited the release of TNF-alpha and IL-1beta in a dose-dependent manner. In conclusion, these results indicate that AKF-PD inhibits the release of the proinflammatory cytokines (TNF-a and IL-1beta) and improves survival during lethal endotoxemia, which suggest this new pyridone agent can be a novel candidate for therapy of septic shock.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / administration & dosage*
  • Cells, Cultured
  • Down-Regulation
  • Endotoxemia / blood
  • Endotoxemia / drug therapy*
  • Endotoxemia / immunology
  • Interleukin-1beta / biosynthesis*
  • Interleukin-1beta / blood
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Macrophages / drug effects*
  • Macrophages / immunology
  • Macrophages / metabolism
  • Macrophages / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Pyridones / administration & dosage*
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • 5-methyl-1-(3-fluorophenyl)-2-(1H)-pyridone
  • Anti-Inflammatory Agents
  • Interleukin-1beta
  • Pyridones
  • Tumor Necrosis Factor-alpha