Protective Effect of Astragaloside IV on Dysfunction of Human Umbilical Vein Endothelial Cells Induced by Hydrogen Peroxide

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( H2O2180 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) + H2O2180 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( e NOS),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 k B-α was decreased and the e NOS 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 e NOS 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: AsⅣ 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 e NOS 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.