The anti-inflammatory effects of ethyl acetate on Lipopolysaccharide/D-galactosamine challenged mice and Lipopolysaccharide activated RAW264.7 cells

Ethyl acetate (EA) is an ordinary organic compound in fruits, wine and cosmetics, and used as a solvent frequently. With the recent observation in our experiment, we suspected that EA could affect immune function, in particular macrophage activity. In this paper, we tested EA’s protect effect against death in Lipopolysaccharide/D-galactosamine (LPS/D-GalN)-induced endotoxic shock model in mice. And also found EA decreased the LPS-induced mRNA expression of mediators of inflammation including cyclooxygenase 2 (COX2), inducible NOS (iNOS), and tumor necrosis factor α (TNF α) in RAW264.7 cells. Consequently, EA decreased the production of, TNF α and the inflammatory agent nitric oxide (NO) in RAW264.7 cells treated with LPS. Other pro-inflammatory cytokines such as IL-1h and IL-6 were similarly decreased by EA treatment of RAW264.7 cells. The potential mechanism may associate with NF-κB activity as we shown. Taken together, these results suggest that EA has anti-inflammatory properties.

► Ethyl acetate inhibited LPS/D-GalN-induced endotoxic shock. ► Ethyl acetate dramatically suppressed the release of TNF-α, IL-β, IL-6 and NO. ► Ethyl acetate down-regulated their gene expression while up-regulating the expression of IL-10. ► Ethyl acetate inhibition of NF-κB activity in LPS-activated RAW264.7 cells.