Protective Effect Of Ethyl Acetate Against Acute Liver Failure In Mice And Underlying Mechanisms

This study aimed to investigate the effect and mechanism of ethyl acetate on LPS-induced inflammation. To evaluate the effect for Ethyl acetate on on D-Galactosamine/ lipopolysaccharide induced acute liver injury in mice. And to explore the mechanism for Ethyl acetate on LPS-stimulated RAW 264.7 Cells.The KM mice were administered saline, vehicle or ethyl acetate (0.4g/kg-1.0g/kg) subcutaneously 30min before GalN/LPS (800mg/100μg)·kg-1 injection, recorded the mortality. Another group were killed at different time point (1h,2h,4h,8h and 12h after GalN/LPS injection), and the Blood, liver samples were collected for analysis. The levels of NO and ALT in serum and liver were detected. A portion of the liver was fixed in 10% neutral formalin, processed by standard histological techniques, stained with hematoxylin and eosin. And study for RAW264.7 cells were pre-treated with vehicle or EA solutions for 20 or 30min before treatment with LPS (800ng/mL). At different time points, the supernatants and cells were collected for immunocytochemistry, ELISA and real-time PCR.In the mice,30min pro-administration of ethyl acetate (0.6g/kg) significantly decreased GalN/LPS -induced mortality from 82.2% to 19.0%. Pretreatment with ethyl acetate inhibited significantly liver damage induced by GalN/LPS. In RAW264.7 cells, we check the activation of nuclear factorκB (NFκB), and found EA could stop NFκB turn into cell nucleus. Elisa and Real time PCR's results shown that EA could significantly lower the pro-inflammatory cytokines and expression (P<0.01 or P<0.05).These results showed that EA may be effective in the treatment of inflammatory conditions.