Astragalus polysaccharide induces anti-inflammatory effects dependent on AMPK activity in palmitate-treated RAW264.7 cells

Astragalus polysaccharide (APS) has been reported to increase insulin sensitization and to ameliorate diabetes in animal models, and studies have demonstrated that this effect may be correlated with its anti-inflammatory roles in vivo and in vitro. However, the potential pharmacological mechanisms of APS in anti-inflammatory regulation are still poorly understood. Herein, RAW264.7 cells treated with APS showed anti-inflammatory effects. Interleukin (IL)-10 protein levels and expression of most of the anti-inflammatory genes, including IL-10, macrophage mannose receptor (MMR), arginase, Dectin-1, YM-1 and YM-2, were significantly increased after treatment with APS for 24 h. Furthermore, to determine whether APS plays a potential role in RAW264.7 cell inflammation, we pretreated RAW264.7 cells with APS in the presence of palmitate. The results showed that APS markedly recovered the impairment of AMPK activity induced by palmitate. Furthermore, APS induced IL-10 protein production and anti-inflammatory gene expression of IL-10, MMR, Dectin-1, arginase, YM-1 and YM-2. Additionally, APS inhibited IL-1 beta protein production and expression of most of the pro-inflammatory genes, such as IL-1 beta, iNOS, MCP-1, IL-6 and CD11c but not tumor necrosis factor (TNF)-alpha. Notably, the effect of APS on inflammatory genes, except for TNF-alpha, was abrogated when AMPK activity was inhibited using a DN-AMPK plasmid. These results suggest that APS effectively ameliorates palmitate-induced pro-inflammatory responses through AMPK activity.