Aim: To investigate the diverse pharmacological actions of astragaloside Ⅳ from the perspective of metabolic syndrome, and to investigate the effect of the drug on 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 determined 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 Ca2+ was labeled with Fluo-3 AM and measured by using a laser scanning confocal microscope. Results:Astragaloside Ⅳ can significantly potentiate insulin-induced preadipocyte differentiation at concentrations of 3, 10, and 30 μg/mL, improve high glucose-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, we found that these effects were partly due to the promotion of PPARγ expression and to the inhibition of abnormal TNF-α-induced intracellular free Ca2+ accumulation in endothelial cells. Conclusion: The diverse pharmacological actions of astragaloside Ⅳ can all be linked to metabolic syndrome pathogenesis. Our study provides a new insight into the mechanism by which astragaloside Ⅳ exerts its effect.