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Astragalus and Panax notoginseng are often combined to treat cerebral infarction.Astragalosides (AST) and Panax notoginseng saponins (PNS) are the effective components with cardio-cerebrovascular pharmacological effects in Astragalus and Panax notoginseng,respectively,they both may antagonize ischemic brain injury.The purpose of this work was to compare the protective effects of AST,PNS and their combinations against cerebral ischemia injury through energy metabolism and neurocyte apoptosis.C56BL/6 mice were randomly divided into sham group,model group,AST (55 mg/kg) group,PNS (57.5 mg/kg)group,small-dose combination group (AST 27.5 mg/kg + PNS 28.75 mg/kg),moderate-dose combination group (AST 55mg/kg + PNS 57.Smg/kg),large-dose combination group (AST 110 mg/kg + PNS 115 mg/kg) and edaravone (4 mg/kg) group,treated for 4 days,then,cerebral ischemia-reperfusion injury was established by bilateral common carotid artery (CCA) ligation for 20 min followed by reperfusion.Our results showed that AST,PNS and their combinations increased the levels of ATP,ADP and Na(+)-K(+)-ATPase activity after reperfusion for 1 h.Twenty-four and 48 h after reperfusion,AST,PNS and the combinationssignificantly increased neurocyte survival and decreased the apoptosis rate as well as down-regulated the expression of phosphorylated c-June N-terminal kinasel/2 (p-JNK1/2),cytochrome C (Cyt C),cysteine aspartic acid-specific protease (caspase)-9 and caspase-3.Furthermore,the effects on energy metabolism and apoptosis were dose dependent among smalllow-dose combination group,moderate-dose combination group and large-dose combination group,and being better in moderate-dose combination group than those in AST or PNS group alone.It suggested that AST,PNS and their combinations had protective effects against cerebral ischemia injury,and the combination between AST and PNS could intensify the effect,the mechanism underlying might be associated with improving energy metabolism,and(_)reducing neurocyte apoptosis via the inhibitions of JNK signaling pathway and mitochondrial apoptosis pathway.