The present study aims to determine the anti-inflammatory activity of DG and elucidate its underlying mechanisms with regards to its molecular basis of action.
The anti-inflammatory effect of DG was studied by using lipopolysaccharide (LPS)-stimulated activation of nuclear factor ¦ÊB (NF¦ÊB) pathway and subsequent production of inflammatory mediators, including nitric oxide (NO), prostaglandin E2 (PGE2), interleukin-1 beta (IL-1¦Â), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-¦Á) and macrophage chemotactic protein-1 (MCP-1), in mouse RAW 264.7 macrophages.
The present study demonstrated that DG could suppress the production of NO and PGE2 through the inhibition of iNOS and COX-2 genes. DG could also inhibit the production of IL-1¦Â, IL-6 and MCP-1, but not TNF-¦Á, through the inhibition of respective mRNA expressions. Further investigations showed the inhibitory effect of DG on activation of IKK¦Á/¦Â and degradation of I¦ÊB¦Á, thus preventing nuclear translocation of NF¦ÊB. All these results suggested the inhibitory effects of DG on the production of inflammatory mediators through the inhibition of the NF¦ÊB pathway.
The inhibitory effects of DG on the production of inflammatory mediators by LPS-stimulated RAW 264.7 macrophages, are accomplished by inhibiting the nuclear translocation of NF¦ÊB through inactivating IKK¦Á/¦Â and preventing degradation of I¦ÊB¦Á.