Acta Pharmacologica Sinica 2006 February; 27 (2): 229-236; doi: 10.1111/j.1745-7254.2006.00243.x

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-g (PPARg) 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)-a-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 PPARg expression and to the inhibition of abnormal TNF-a-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.

Keywords: astragaloside IV; metabolic syndrome X; insulin resistance; peroxisome proliferator-activated receptors; apoptosis; calcium