Inhibitory effects of saponins from Anemarrhena asphodeloides Bunge on the growth of vascular smooth muscle cells.

OBJECTIVE: To investigate the effects of saponins from Anemarrhena asphodeloides Bunge (SAaB) (Botanical Name: Anemarrhena Asphodeloidis Rhizoma) on the growth of vascular smooth muscle cells (VSMCs). METHODS: Cell proliferation was measured by a newly developed cell proliferation reagent, WST-1. Cell apoptosis was assayed by flow cytometry through detecting annexin V. Nitric oxide production was evaluated using confocal laser scanning microscopy with diaminofluorescein diacetate (DAF-2, DA). Cell aldose reductase (AR) activity, as well as the effect of Epalrestat and interleukin-1beta were also explored. RESULTS: WST assay showed that cell proliferation induced by serum was significantly inhibited by SAaB (P<0.01). Flow cytometry analysis revealed that SAaB could enhance apoptotic rate of VSMCs (P<0.01). Nitric oxide production was significantly enhanced after administration of SAaB and interleukin-1beta. Moreover, AR activity of VSMCs was also remarkably inhibited by both SAaB and Epalrestat (P<0.01). CONCLUSION: SAaB can inhibit proliferation and enhance apoptosis of VSMCs. It may protect vascular cells by inhibiting VSMC proliferation and augmenting apoptotic rate of VSMCs via NO-dependent pathway.

A preadipocyte differentiation assay as a method for screening potential anti-type II diabetes drugs from herbal extracts.

A cell-based method for screening drug candidates from herbal extracts that have possible anti-type II diabetic effects was established. The differentiation of preadipocytes into adipocytes was used as a sensitive primary indicator of a drug's potential effect on type II diabetes. We established a quantitative method by using a computer image analysis system for assessing the morphological alterations. The assay was validated by screening compounds extracted from Chinese herbs and the known drug rosiglitazone for their capability of modulating PPARgamma gene expression and glucose uptake by adipocytes. Two drug candidates having possible anti-type II diabetic effects were identified.

Effects of astragaloside IV on pathogenesis of metabolic syndrome in vitro.

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-(3)H]-deoxyglucose into the cells. The concentrations of peroxisome proliferator-activated receptor-gamma (PPARgamma) 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 microg/mL, improve high glucose-induced insulin resistance in adipocytes at a concentration of 30 microg/mL, and prevent tumor necrosis factor (TNF)-alpha-induced apoptosis and viability loss at concentrations of 10 and 30 microg/mL, and 30 microg/mL, respectively, in endothelial cells. Furthermore, we found that these effects were partly due to the promotion of PPARgamma expression and to the inhibition of abnormal TNF-alpha-induced intracellular free Ca(2+) 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.

The study of anti-metabolic syndrome effect of puerarin in vitro.

Puerarin is an isoflavone extracted from Chinese plant, Pueraria lobata (Wild.) Ohwi. It has been reported to have comprehensive pharmacological action in treatment of diabetes and cardiovascular diseases. The purpose of this study was to link the scattered effects of puerarin and to find the common mechanisms underlying. We investigated the effect of puerarin on the pivotal common pathogenic factors of metabolic syndrome, which includes obesity, Type II diabetes and cardiovascular diseases. Recently, a large body of evidence indicates that there is a complicated interplay among insulin resistance, adipocytes and endothelial dysfunction that links the abnormalities of metabolic syndrome. Results of present study showed that puerarin could potentiate insulin-induced preadipocyte differentiation, promote glucose-uptake of adipocytes that have been induced insulin resistance by high glucose, and prevent TNF-a-induced apoptosis and viability loss of endothelial cells. Furthermore, we found that these effects are probably due to promote PPARgamma expression and partly through inhibiting abnormal TNF-a-induced intracellular-free Ca(2+) accumulation of endothelial cells. Overall, our synthetical study links the comprehensive pharmacological actions of puerarin to the recognized common pathogenesis of metabolic syndrome, and provides a new insight into the mechanism of puerarin effect.