Effects of astragaloside IV on pathogenesis of metabolic syndrome in vitro
Abstract
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.
Keywords:
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.