【Objective】To explore the effect and mechanism of ginsenoside Rb1 on replicative senescence of endothelial cells.【Methods】Establish the replicative senescence model of primary human umbilical vein endothelial cells（HUVEC）：the morphological change of the cells，the proportion of senescence-associated β-galactosidase（SA-β-Gal politive cells and the plasminogen activator inhibitor1（PAI-1）expression were detected to assessthe senescence model； replicative senescence model cells were divided into 0，20，40，80 and 100 μmol/L Rb1 group，SA-β-Galstaining positive cells and PAI-1 protein level were measured after treatment of senescent cells with different concentrations of Ginsenoside Rb1 for 48h，3 multiplepores in each group. NF-κBp65 and p-NF-κBp65 protein expression in normal cell group（CPDL2HUVEC），model group（senescent cell group）and ginsenoside Rb1 group were detected by RT-PCR，3 multiplepores in each group；the markers of oxidative stress and inflammation in cell culture solution were measured，3 multiplepores in each group.【Results】HUVEC with CPDL16 have been chosen as the replicative senescence model in this research. Compared with the 0 μmol/L Rb1 group，the SA-β-Gal positive cells and protein expression level of PAI1 were significantly decreased（P<0.001）in 80 μmol/L Rb1 group. Compared with the control group，the production of MDA，IL-6 and TNF-α and NF-κBp65 activity were significantly increased（P<0.001）in model group，but the activity of SOD was significantly decreased（P<0.001）.However，Compared with the model group，the activity of SOD was increased（P<0.05），the production of MDA，IL-6 and TNF-α were decreased（P<0.05）and the activity of NF-κB p65 was decreased（P<0.001）in 80 μmol/L Rb1 group.【Conclusions】Ginsenoside Rb1 ameliorates the replicative senescence of endothelial cells by suppressing inflammation and oxidative stress via NF-κBp65.