Experimental Study on the Regulation of PI3K/AKT Pathway by Momordicoside L Promoting Endothelial Progenitor Cell Proliferation and Endothelial Function
HUANG Jianming
LIU Di
JIN Daoqun
ZHU Dingjun
Abstract：Objective:To explore the effect of Momordicoside L on endothelial progenitor cells(EPC)proliferation and endothelial function and its mechanism.Methods:Peripheral blood EPCs were isolated,cultured,and identified in vitro.After EPC was treated with different concentrations of Momordicoside L for 24 h,cell viability was detected by cell count(CCK-8).By AutoDock Tools 5.6 software,the molecular docking was performed by blind docking method with phosphatidylinositol 3-kinase(PI3K)and protein kinase B(AKT)as receptors,and the drug molecule Momordicoside L as ligand.The cell viability and the expressions of phosphorylated PI3K(p-PI3K),phosphorylated AKT(p-AKT)and phosphorylated endothelial nitric oxide synthase(p-eNOS)in each group were detected,when EPC was treated with PI3K/AKT inhibitor LY294002 and the optimal concentration of Momordicoside L alone or simultaneously for 24 h.Results:Compared with control group,Momordicoside L could promote EPC proliferation in a dose-dependent manner,and 40μmol/L was the optimal concentration.Compared with the control group,LY294002 could down-regulate EPC cell viability,and Momordicoside L could up-regulate EPC cell viability.Compared with Momordicoside L group,the co-administration of Momordicoside L and LY294002 decreased cell viability.Molecular docking results showed that Momordicoside L had direct interaction with PI3K and AKT,and could form a stable lock key structure.Compared with the control group,LY294002 significantly down-regulated the protein levels of p-PI3K,p-AKT and p-eNOS.Momordicoside L up-regulated the protein levels of p-PI3K,p-AKT and p-eNOS.Compared with the Momordicoside L group,the administration of Momordicoside L and LY294002 decreased the protein levels of p-PI3K,p-AKT and p-eNOS.Conclusion:Momordicoside L could regulate the proliferation ability of EPC through the PI3K/AKT signaling pathway,and then up-regulate the activation level of endothelial nitric oxide synthase(eNOS)to promote endothelial function of EPC.
Keywords：endothelial progenitor cellsMomordicoside Lcell proliferationendothelial functionexperimental study
Publication Date：2024-05-16
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 1768-1772 )