18β-Glycyrrhetinic acid inhibits oxLDL-induced apoptosis of vascular endothelial cells through PGK1 glycolysis pathway
The molecular mechanism of 18β-glycyrrhetinic acid(GA)inhibiting oxidative low-density lipoprotein-induced ap-optosis 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 40μmol/L)and PGK1 agonists were given different concentrations to intervene.The key glycolytic enzyme PGK1,glucose trans-porter 1(GLUT1),hexokinase 2(HK2)and pyruvate kinase M2 were detected by Western blot.PKM2 and apoptosis-related Bax,Bc12,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 de-creased,and protein expression levels of PGK1,GLUT1,HK2,PKM2,Bax,cleaved Caspase-3 and cleaved Caspase-9 were in-creased(P＜0.05).Compared with oxLDL group,glucose consumption and lactate secretion of endothelial cells in GA treat-ment group(10,20 and 40 μmol/L)were increased,and protein expression levels of PGK1,GLUT 1,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 vas-cular endothelial cells by inhibiting PGK1-mediated glycolysis pathway.
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维普
