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Aim of study:Hepatic ischemia/reperfusion (I/R),the leading cause of severe liver injury,is characterized by hepatocyte apoptosis and chronic inflammation.However,there were no effective approaches to prevent the resultant pathological conditions induced by hepatic I/R.Ginsenoside Rgl,the major active ingredient of Panax genus,exhibits significant anti-apoptotic and anti-inflammatory properties;however,the impact of ginsenoside Rgl on hepatic I/R remains largely unknown.However,there were no effective approaches to prevent the resultant pathological conditions induced by hepatic I/R.Ginsenoside Rgl,the major active ingredient of Panax genus,exhibits significant anti-apoptotic and anti-inflammatory properties;however,the impact of ginsenoside Rgl on hepatic I/R remains largely unknown.Here,we evaluated the effect and molecular events underlying the regulation of hepatic I/R-induced liver damage by ginsenoside Rgl.Material and methods:The modulation of ginsenoside Rg1 were assayed in a mouse hepatic I/R model with 60 min of ischemia followed by 0,6,12 or 24 h of reperfusion.Ginsenoside Rgl (20 mg/kg/d) was intraperitoneally administered 7 d prior to hepatic ischemia.Further,to identify which hepatic I/R processes was influenced by ginsenoside Rg1,in vitro hypoxia/reoxygenation-or lipopolysaccharide-induced hepatocyte damage models were also established.Results:Administration of ginsenoside Rg1 significantly diminished liver dysfunction induced by hepatic I/R and suppressed liver necrosis,inflammatory responses and cell death.Mechanistic investigations dem onstrated the activation of proteins in c-Jun N-terminal kinase (JNK) signaling pathway was dramatically inactivated by ginsenoside Rg1.Our in vitro observations indicated that only the inflammation-,rather than oxidative stress-induced cytotoxicity was significantly inhibited by ginsenoside Rgl,which was almost completely abolished by anisomycin,a specific JNK activator.Conclusions:Ginsenoside Rgl exerts protective effects against hepatic I/R-derived liver damage through inhibiting cell apoptosis and inflammation in a JNK signaling-dependent manner.Our findings suggest the promising possibility of ginsenoside Rgl to be developed as an effective agent for treating hepatic I/R injury and related liver damage.