Inhibitory effect of Astragalus polysaccharides on lipopolysaccharide-induced TNF-a and IL-1β production in THP-1 cells

Molecules. 2012 Mar 12;17(3):3155-64. doi: 10.3390/molecules17033155.


Astragalus polysaccharides (APS), one of main bioactive components in Astragalus membranaceus Bunge, has been reported to possess anti-inflammatory activities, but the molecular mechanisms behind this activity are largely unknown. This study aimed to investigate expression of inflammatory cytokines and the MAPK/NF-κB pathway in human THP-1 macrophages induced by lipopolysaccharide (LPS). The results showed that the concentrations of TNF-a and IL-1β released from LPS stimulated THP-1 cells increased significantly compared to control (p < 0.01). After treatment with APS, the TNF-a and IL-1β levels were significantly lower than those in the LPS group (p < 0.05). The mRNA expression of TNF-a and IL-1β were also inhibited. Mechanistic studies indicated that APS strongly suppressed NF-κB activation and down-regulated the phosphorylation of ERK and JNK, which are important signaling pathways involved in the production of TNF-a and IL-1β, demonstrating that APS could suppress the production of TNF-a and IL-1β by LPS stimulated macrophages by inhibiting NF-κB activation and ERK and JNK phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents / pharmacology*
  • Astragalus propinquus / chemistry*
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Humans
  • Interleukin-1beta / biosynthesis*
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Lipopolysaccharides / pharmacology
  • MAP Kinase Signaling System / drug effects
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / metabolism
  • Phosphorylation / drug effects
  • Polysaccharides / pharmacology*
  • Transcription, Genetic / drug effects
  • Tumor Necrosis Factor-alpha / biosynthesis*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism


  • Anti-Inflammatory Agents
  • Interleukin-1beta
  • Lipopolysaccharides
  • NF-kappa B
  • Polysaccharides
  • Tumor Necrosis Factor-alpha
  • Mitogen-Activated Protein Kinases