Astragalus polysaccharide attenuates lipopolysaccharide-induced inflammatory responses in microglial cells: regulation of protein kinase B and nuclear factor-κB signaling

Inflamm Res. 2015 Apr;64(3-4):205-12. doi: 10.1007/s00011-015-0798-9. Epub 2015 Feb 11.


Objectives and design: Microglia play an important role in immune and inflammatory responses in the central nervous system. Astragalus polysaccharide (APS) has been reported as an immune stimulant for various inflammation-associated diseases in vivo. The present study investigated the effects of APS on lipopolysaccharide-stimulated inflammatory responses in microglial cells.

Materials and methods: Cultured BV2 microglial cells were pre-treated with APS (0-200 μg/ml) prior to lipopolysaccharide (50 ng/ml) stimulation. The production of proinflammatory mediators including inducible nitric oxide synthase (iNOS)/nitric oxide (NO), cyclooxygenase-2 (COX-2)/prostaglandin E (PGE2), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were evaluated.

Results: APS dose-dependently reduced lipopolysaccharide stimulated nitric oxide and PGE2 production, as well as iNOS and cyclooxygenase-2 gene expression. It also attenuated proinflammatory cytokines IL-1β and TNF-α generation. In addition, APS inhibited nuclear factor-κB translocation by blockade of IκB degradation and suppressed protein kinase B phosphorylation in lipopolysaccharide-stimulated cells.

Conclusions: The inhibitory effects of APS on lipopolysaccharide-stimulated inflammatory mediator production in microglia are associated with suppression of nuclear factor-κB and protein kinase B signaling pathways. APS may offer therapeutic potential for treating inflammatory and neurodegenerative diseases accompanied with microglial activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astragalus Plant* / metabolism
  • Cells, Cultured
  • Cyclooxygenase 2 / metabolism
  • Dinoprostone / metabolism
  • Inflammation / chemically induced
  • Inflammation / metabolism
  • Inflammation / prevention & control*
  • Interleukin-1beta / metabolism
  • Lipopolysaccharides / adverse effects
  • Lipopolysaccharides / pharmacology
  • Mice
  • Microglia / drug effects
  • Microglia / metabolism*
  • Microglia / pathology
  • Models, Animal
  • NF-kappa B / metabolism*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Polysaccharides / metabolism
  • Polysaccharides / pharmacology*
  • Polysaccharides / therapeutic use*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / drug effects*
  • Tumor Necrosis Factor-alpha / metabolism


  • Interleukin-1beta
  • Lipopolysaccharides
  • NF-kappa B
  • Polysaccharides
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • Proto-Oncogene Proteins c-akt
  • Dinoprostone