Ginsenoside Rg1 Protects Endothelial Cell Injury Induced By Doxorubicin Through Antioxidant And Apoptosis

ObjectiveTo investigate the protective effect of ginsenoside Rg1 on doxorubicin-induced vascular endothelial cells and its mechanism.MethodsHuman Umbilical Vein Endothelial Cells(HUVECs)were cultured in vitro.The experiments were divided into normal control group,doxorubicin treatment group(0.5μg/m L),and doxorubicin + Rg1 treatment group(0.5μg/m L+200μg/m L).The effects of ginsenoside Rg1 on the proliferation,migration,and tubule formation of vascular endothelial cells after doxorubicin injury were detected by MTT,scratches,and tubule formation experiments.The effects of ginsenoside Rg1 on apoptosis of vascular endothelial cells after doxorubicin injury was detected by Hochest33342 fluorescence staining and flow cytometry.The effects of ginsenoside Rg1 on Reactive Oxygen Species(ROS)and NO after doxorubicin injury were detected by Nitric Oxide(NO)fluorescent probes(DAF-FM DA)and superoxide anion fluorescent probes(DHE).The expression of Bcl-2,p-AKT,p-ERK and p-e NOS in vascular endothelial cells after doxorubicin injury was detected by western blot,and the protective mechanism of ginsenoside Rg1 against doxorubicin injury was further investigated.ResultsCompared with the normal control group,the cell survival rate,migration rate and tubule formation in the doxorubicin-treated group were significantly reduced(P<0.05),and the NO content was reduced(P<0.05);The fluorescence intensity and apoptosis rate of Hoeches33342 staining increased(P<0.05),and the intracellular ROS content increased(P<0.05),which significantly decreased the expression of Bcl-2,p-AKT,p-ERK and p-e NOS.Compared with the doxorubicin-treated group,ginsenoside Rg1 promoted vascular endothelial cell proliferation(P<0.05),migration and tubule formation(P<0.05),NO(P<0.05),and reduced vascular endothelial cell decay induced by doxorubicin the death and ROS content(P<0.05)significantly increased the expression of Bcl-2,p-AKT,p-ERK and p-e NOS proteins in vascular endothelial cells.ConclusionsThe results suggest that ginsenoside Rg1 can reduce the damage of vascular endothelial cells caused by doxorubicin,and its mechanism may reduce the damage of vascular endothelial cells by doxorubicin by increasing Bcl-2,p-AKT,p-ERK,p-e NOS.Therefore,it provides a new target for ginsenoside Rg1 in the treatment of doxorubicin-induced heart injury.