Intracerebroventricular ginsenosides are antinociceptive in proinflammatory cytokine-induced pain behaviors of mice

Arch Pharm Res. 2008 Mar;31(3):364-9. doi: 10.1007/s12272-001-1165-x. Epub 2008 Apr 13.

Abstract

Several ginsenosides (Rb1, Rb2, Rc, Rd, Re, Rf, Rg1 and Rg3) are neuroprotective and antinociceptive agents. In this study, we assessed the effects of these ginsenosides following intracerebroventricular (i.c.v.) administration on the nociceptive behaviors induced by intrathecal injection of pro-inflammatory cytokines (tumor necrosis factor-a (TNF-alpha), interleukin-1 beta (IL-1 beta), and interferon-gamma (IFN-gamma)). The ginsenosides, Rb1, Rb2, Rc, Rd, Re, Rf and Rg1, significantly attenuated the nociceptive behavior induced by TNF-alpha, IL-1 beta, and IFN-gamma injection, but ginsenoside-Rg3 did not. These results suggest that several ginsenosides may regulate the nociceptive processing induced by pro-inflammatory cytokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analgesics / administration & dosage*
  • Animals
  • Behavior, Animal / drug effects*
  • Cytokines / administration & dosage
  • Cytokines / metabolism*
  • Disease Models, Animal
  • Ginsenosides / administration & dosage*
  • Inflammation Mediators / administration & dosage
  • Inflammation Mediators / metabolism*
  • Injections, Intraventricular
  • Injections, Spinal
  • Interferon-gamma / metabolism
  • Interleukin-1beta / metabolism
  • Male
  • Mice
  • Mice, Inbred ICR
  • Pain / metabolism
  • Pain / prevention & control*
  • Pain Measurement
  • Pain Threshold / drug effects
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Analgesics
  • Cytokines
  • Ginsenosides
  • Inflammation Mediators
  • Interleukin-1beta
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma