Aim:To investigate the diverse pharmacological actions of astragaloside IV fromthe perspective of metabolic syndrome,and to investigate the effect of the drugon the pathogenesis of metabolic syndrome.Methods:Adipogenesis was usedas an indicator of the effect of astragaloside Ⅳ on preadipocyte differentiation,and was measured by using an oil red O assay.Glucose uptake was determined bymeasuring the transport of [2-~3H]-deoxyglucose into the cells.The concentrationsof peroxisome proliferator-activated receptor-γ(PPARγ)and aP2 mRNA were de-termined by using reverse transcription-polymerase chain reaction.Apoptosisand viability loss of endothelial cells were detected by using flow cytometry andthe WST-1 assay,respectively.Intracellular free Ca~(2+) was labeled with Fluo-3 AMand measured by using a laser scanning confocal microscope.Results:Astragaloside Ⅳ can significantly potentiate insulin-induced preadipocyte differ-entiation at concentrations of 3,10,and 30 μg/mL,improve high glucose-inducedinsulin resistance in adipocytes at a concentration of 30 μg/mL,and prevent tumornecrosis factor(TNF)-α-induced apoptosis and viability loss at concentrations of10 and 30 μg/mL,and 30 μg/mL,respectively,in endothelial cells.Furthermore,wefound that these effects were partly due to the promotion of PPARγ expressionand to the inhibition of abnormal TNF-α-induced intracellular free Ca~(2+) accumula-tion in endothelial cells.Conclusion:The diverse pharmacological actions ofastragaloside 1V can all be linked to metabolic syndrome pathogenesis.Our studyprovides a new insight into the mechanism by which astragaloside Ⅳ exerts itseffect. Aim: To investigate the diverse pharmacological actions of astragaloside IV from the perspective of metabolic syndrome, and to investigate the effect of the drugon the pathogenesis of metabolic syndrome. Methods: Adipogenesis was used as an indicator of the effect of astragaloside IV on preadipocyte differentiation, and was measured by using an oil red O assay. Glucose uptake was determined by measuring the transport of [2- ~ 3H] -deoxyglucose into the cells. The concentrations of peroxisome proliferator-activated receptor-γ (PPARγ) and aP2 mRNA were de-termined by using reverse transcription-polymerase chain reaction. Apoptosis and viability loss of endothelial cells were detected by using flow cytometry and the WST-1 assay, respectively. Intracellular free Ca 2+ was labeled with Fluo-3 AMand measured by using a laser scanning confocal microscope Results: Astragaloside IV can significantly potentiate insulin-induced preadipocyte differ- entiation at concentrations of 3, 10, and 30 μg / mL, improve high gl ucose-induced insulin resistance in adipocytes at a concentration of 30 μg / mL, and prevent tumor necrosis factor (TNF) -α-induced apoptosis and viability loss at concentrations of 10 and 30 μg / mL, and 30 μg / mL, respectively, in endothelial cells .Furthermore, wefound that these effects were partly due to the promotion of PPARγ expression and to the inhibition of abnormal TNF-α-induced intracellular free Ca 2+ accumulation in endothelial cells. Conlusion: The diverse pharmacological actions of astragaloside 1V can all be linked to metabolic syndrome pathogenesis. Our studyprovides a new insight into the mechanism by which astragaloside Ⅳ exerts itseffect.