Protective effects of 20 (R)-ginsenoside Rg_3 on human umbilical vein endothelial cell injury induced by tumor necrosis factor-α

Objectives To investigate the preventive effect of 20(R)-ginsenoside Rg3 on human umbilical vein endothelial cell (HUVEC) injury and its preliminary mechanism.Methods Tumor necrosis factor-α(TNF-α)was used to injure HUVEC in vitro.Cell viability was assessed with methyl thiazolyl tetrazolium (MTT) assay.The cultured cells were loaded by Fura-2/AM and the change of cytosolic calcium concentration in HUVEC was measured by fluorospectrophotometry.The concentrations of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1(PAI-1) in the supernatant were measured by enzyme linked immunosorbent assay (ELISA).Results (1)The better condition of TNF-α injuring HUVEC was 20 μg/Lof the final concentration stimulating for 24 h.(2)20 μg/Lof TNF-α significantly decreased the absorbance values of HUVEC.However,10-80μmol/L of 20(R)-ginsenoside Rg3 markedly elevated the absorbance values of HUVEC as compared with model group (P0.01).(3)TNF-α increased the cytosolic calcium concentration compared with normal group(P0.01).Calecium concentration was significantly decreased by 10-80μmol/L of 20(R)-ginsenoside Rg3 when compared with model group (P0.01) and its half maximal inhibitory concentration (IC50) was 67.2μmol/L.(4)As compared with the control group,stimulated by TNF-α(20 μg/Lfor 24 h),the concentrations of t-PA were significantly decreased in supernatant of cultivated cells,while PAI-1 was significantly increased.20(R)-ginsenoside Rg3 (10-80μmol/L)significantly reduced the concentrations of PAI-1,while elevated t-PA level as compared with model group(P0.01).IC50 of 20(R)-ginsenoside Rg3 for PAI-1 was 36.9μmol/L.Conclusions 20(R)-ginsenoside Rg3 can protect cultured HUVEC injury induced by TNF-α.The mechanism may be associated with suppressing the mobilization of cytosolic calcium,inhibiting the generation of PAI-1,and elevating t-PA level.