The molecular mechanism of 18β-glycyrrhetinic acid (GA) inhibiting oxidative low-density lipoprotein-induced apoptosis of vascular endothelial cells was studied based on the phosphoglycerate kinase-1-mediated glycolysis pathway.oxLDL (100 mg/L) injury was used to establish the human aortic endothelial cell injury model in vitro,and GA (10,20 and 40 μmol/L) and PGK1 agonists were given different concentrations to intervene.The key glycolytic enzyme PGK1,glucose transporter 1(GLUT1),hexokinase 2 (HK2) and pyruvate kinase M2 were detected by Western blot.PKM2 and apoptosis-related Bax,Bcl2,Caspase-3 and Caspase-9 protein expression levels were detected by colorimetric assay.The results showed that compared with the control group,glucose consumption and lactate secretion of endothelial cells in oxLDL group were decreased,and protein expression levels of PGK1,GLUT1,HK2,PKM2,Bax,cleaved Caspase-3 and cleaved Caspase-9 were increased (P<0.05).Compared with oxLDL group,glucose consumption and lactate secretion of endothelial cells in GA treatment group (10,20 and 40 μmol/L) were increased,and protein expression levels of PGK1,GLUT1,HK2,PKM2,Bax,Caspase-3 and Caspase-9 were decreased (P<0.05).The effect of GA on oxLDL-induced apoptosis of vascular endothelial cells was reversed after addition of PGK1 agonist.These results indicated that GA inhibited OXLDL-induced apoptosis of vascular endothelial cells by inhibiting PGK1-mediated glycolysis pathway.