Escin protects against acetaminophen-induced liver injury in mice via attenuating inflammatory response and inhibiting ERK signaling pathway.

Acetaminophen (APAP) overdose may lead to the formation of oxidative stress, hepatocyte apoptosis and necrosis, and, eventually result in acute liver failure. Escin, a major extracted component of , reportedly exerts anti-inflammatory, anti-edematous and anti-oxidant properties. Previous studies have demonstrated these protective effects of extracts on ischemia/reperfusion intestinal injury and endotoxin-induced lung injury. In this study, we aimed to evaluate the effect of escin on APAP-induced liver injury in mice. Mice were intraperitoneally administrated with APAP (300 mg/kg) or an equal volume of saline (control), followed by a treatment with various concentrations of escin (0, 0.5, 1, 2 and 4 mg/kg) for 30 min. The animals were sacrificed 16 h following APAP administration for serum and liver tissue assay. Escin treatment attenuated the damage of APAP-induced liver injury in a dose-dependent manner (0.5-4 mg/kg). Escin also attenuated the hepatic myeloperoxidase (MPO) activity and hepatic pro-inflammatory cytokines (i.e., TNF-α, IL-1β, IL-6 and IL-17). Furthermore, escin treatment decreased the hepatic phosphorylation expression of extracellular signal-regulated kinase (ERK). Our data indicates that escin shows protective effects on APAP-induced hepatotoxicity in a dose-dependent manner through anti-inflammatory mechanism and the inhibition of ERK signaling pathway.