Liquiritin promotes angiogenesis of human umbilical vein endothelial cells after injury through up-regulating pyruvate kinase M2 expression
Objective:To investigate whether liquiritin(LIQ)up-regulation of pyruvate kinase M2(PKM2)on the angiogenesis of human umbilical vein endothelial cells(HUVECs)induced by hydrogen peroxide(H2O2)and its possible mechanism.Methods:HUVECs were damaged by H2O2,and the cells were di-vided into the control group,H2O2 group,H2O2+LIQ group,H2O2+LIQ+Shikonin(PKM2 inhibi-tor)group,and H2O2+LIQ+Static(STAT3 inhibitor)group.Cell migration and tubular formation ability were detected by cell scratch and lumen formation assay.Western Blot was used to detect the ex-pression of key angiogenic proteins VEGF and FGF2,and the expression of proteins,PKM2 and phos-phorylationp-PKM2(p-PKM2),and PKM2 downstream kinase STAT3/p-STAT3.Results:Com-pared with the H2O2 group,LIQ treatment significantly improved cell migration and tubeforming abili-ty,and the expression levels of VEGF,FGF2,PKM2,and p-PKM2.LIQ up-regulated PKM2 ex-pression and significantly increased the expression levels of STAT3 and p-STAT3.Compared with those in the H2O2+LIQ group,cell migration,and tube-forming ability were significantly decreased af-ter PKM2 or STAT3 inhibition,and the increasing trend of VEGF,FGF2,STAT3,and p-STAT3 proteins was reversed.Conclusion:LIQ can activate the STAT3 signaling pathway by upregulating PKM2 expression to promote H2O2-induced angiogenesis in HUVECs.
Pyruvate Kinase M2LiquiritinUmbilical Vein Endothelial CellsAngiogenesisSTAT3 Signal Pathway
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