Objective: To explore the protective effects of astragaloside IV (As IV) on the dysfunction of human umbilical vein endothelial cells (HUVECs) induced by hydrogen peroxide and the underlying mechanism. Method: Human umbilical vein endothelial cells were cultured in vitro and divided into five groups including normal

model(H2O2 180 μmol · L-1)

As IV(25 μmol · L-1)+H2O2(180 μmol · L-1)

As Ⅳ(50 μmol · L-1)+H2O2(180 μmol · L-1)

As IV(100 μmol · L-1)+H2O2 180 μmol · L-1.The cell viability was evaluated by MTT assay

endothelial superoxide anion generation was determined by staining of cells with fluorescent-labeled dihydroethidium. Western blot were used to quantify intracellular protein expression of nuclear factor-κB(NF-κB)p65

IκB-α and endothelial nitric oxide synthase (eNOS)

the expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the extracellular fluid by enzyme-linked immunosorbent assay (ELISA). Result: Compared with the normal group

the cell viability of model group were decreased remarkably

the intracellular superoxide anion generation were increased significantly

the protein expression of p65 was increased while the kB-α was decreased and the eNOS was increased

the production of TNF-α and IL-6 in the extracellular fluid were increased obviously(P <0.01). Comparing with the model group

the cell viability was increased

the intracellular superoxide anion generation was decreased

the protein expression of p65 was decreased

while the IκB α was increased and the eNOS was decreased

the production of TNF-α and IL-6 was decreased in 3 dose groups of As Ⅳ

and the differences showed a dose-dependent(P <0.05). Conclusion: As Ⅳ has protective effects on the dysfunction of human umbilical vein endothelial cells induced by H2O2.The mechanism may be related to reducing superoxide anion production

inhibiting eNOS uncoupling which could produce superoxide anion

thus attenuating oxidative stress and reducing the expression of NF-κB and related inflammatory cytokine. Consequently As Ⅳ could protect human umbilical vein endothelial cells from damage induced by H2O2.