Inhibition of TLR ligand- and interferon gamma-induced murine microglial activation by Panax notoginseng

J Neuroimmune Pharmacol. 2012 Jun;7(2):465-76. doi: 10.1007/s11481-011-9333-0. Epub 2011 Dec 21.

Abstract

Among the many products which influence microglial activation and resulting neuroinflammation, herbal medicine has recently drawn much attention due to its immunomodulatory and neuroprotective activities. The purpose of the current study was to investigate the effects of an extract of Panax notoginseng (NotoG™) on TLR ligand- and IFNγ-induced activation in N9 and EOC20 microglial cells lines. NotoG suppressed microglial activation as measured by reduced expression of accessory molecules (CD40 and CD86), decreased production of inflammatory mediators (IL-6 and TNFα), and diminished release of antibacterial products (nitric oxide). Furthermore, this immunosuppressive activity was neither dependent on the glucocorticoid receptor, nor the result of a single ginsenosides (Rb1, Rg1, or Re), which are the major active constituents of the whole extract. NotoG and select ginsenosides may therefore be of therapeutic benefit in treating or preventing neurodegenerative diseases such as multiple sclerosis and parkinson's disease.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Cell Line
  • Cytokines / analysis
  • Cytokines / biosynthesis
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Ginsenosides / pharmacology*
  • Immunologic Factors / pharmacology*
  • Interferon-gamma / pharmacology
  • Ligands
  • Mice
  • Microglia / drug effects*
  • Microglia / immunology
  • Panax notoginseng / chemistry
  • Plant Extracts / pharmacology*
  • Plant Roots / chemistry
  • Toll-Like Receptors / immunology

Substances

  • Cytokines
  • Ginsenosides
  • Immunologic Factors
  • Ligands
  • Plant Extracts
  • Toll-Like Receptors
  • ginsenoside Rb1
  • Interferon-gamma
  • ginsenoside Rg1