Effects of 2,3,4′,5-Tetrahydroxystilbene 2- O -β- D -Glucoside on Vascular Endothelial Dysfunction in Atherogenic-Diet Rats
Department of Pharmacology, School of Medicine, Nantong University, Nantong, P. R. China. Planta Medica
(Impact Factor: 2.15).
05/2009; 75(11):1209-14. DOI: 10.1055/s-0029-1185540
2,3,4',5-Tetrahydroxystilbene 2- O-beta- D-glucoside (TSG), an active component extracted from Polygonum multiflorum, has been found to have an anti-atherosclerotic effect. The aim of this study was to investigate whether the TSG could prevent the development of atherosclerosis through influencing endothelial function in atherogenic-diet rats and to explore the possible mechanisms. Vascular endothelial dysfunction was assessed using isolated aortic ring preparation, transmission electron microscopy of the aorta, and levels of nitrate/nitrite (NOx) in serum and aorta. Endothelial nitric oxide (NO) synthase (eNOS) and inducible NO synthase (iNOS) mRNA and protein expression were also measured. After 12 weeks treatment, TSG improved acetylcholine-induced endothelium-dependent relaxation, prevented intimal remodeling, inhibited the decreased NOx content in serum and aorta in atherogenic-diet rats. Furthermore, the observed decreased eNOS mRNA and protein expression and increased iNOS mRNA and protein expression in atherogenic-diet rats were attenuated by TSG treatment. These results suggest that TSG could restore vascular endothelial function, which may be related to its ability to prevent changes of eNOS and iNOS expression, leading to preservation of NO bioactivity.
Available from: link.springer.com
- "A monomer of stilbene from a traditional Chinese herbal medicine polygonummultiflorum, 2,3,4’ ,5-tetrahydroxystilbene 2-O-β-D-glucoside (TSG), has also been found to attenuate inflammatory responses . Its anti-inflammatory function was supported by the following evidence: 1) TSG suppresses COX-2 expression in a carrageenin-induced rat paw edema model ; 2) TSG reduces NO levels in serum and the aorta in atherosclerotic rats ; and 3) TSG decreases iNOS expression and infarct volume in the ischemic brain . In the third case, the effect of TSG was explained by the suppression of NF-κB nuclear translocation in neurons but not in microglia . "
[Show abstract] [Hide abstract]
ABSTRACT: Induction of pro-inflammatory factors is one of the characteristics of microglia activation and can be regulated by numerous active components of Chinese traditional herbs. Suppression of pro-inflammatory factors is beneficial to alleviate microglia-mediated cell injury. The present study aims to investigate the effect and possible mechanism of 2,3,4',5-tetrahydroxystilbene 2-O-beta-D-glucoside (TSG) on LPS-mediated induction of pro-inflammatory factors in microglia.
Western blot, ELISA, and Hoechst 33258 were used to measure the protein expression, TNF-alpha/IL-6 content, and apoptotic nuclei, respectively. The mRNA level was measured by real time-PCR. Nitric oxide (NO) content, lactate dehydrogenase (LDH) content, and NF-kappaB binding activity were assayed by commercial kits.
TSG reduced iNOS protein expression as well as TNF-alpha, IL-6, and NO content in LPS-stimulated BV-2 cells. TSG attenuated the increase in apoptotic nuclei, caspase-3 cleavage, and LDH content induced by BV-2 cell-derived conditioned medium in primary hippocampal neurons. Mechanistic studies showed that TSG reduced the mRNA level of iNOS, TNF-alpha, and IL-6. TSG failed to suppress IkappaB-alpha degradation, NF-kappaB phosphorylation and nuclear translocation, and ERK1/2, JNK, and p38 phosphorylation. TSG, however, markedly reduced the binding of NF-kappaB to its DNA element. Chromatin immunoprecipitation (ChIP) assays confirmed that TSG reduced NF-kappaB binding to the iNOS promoter. These findings were ascertained in primary microglia where the LPS-induced increase in iNOS expression, NO content, apoptotic nuclei, and NF-kappaB binding to its DNA element were diminished by TSG.
These studies demonstrate that TSG attenuates LPS-mediated induction of pro-inflammatory factors in microglia through reducing the binding activity of NF-kappaB. This might help us to further understand the pharmacological role of TSG in inflammatory response in the central nervous system.
Journal of Neuroinflammation 10/2013; 10(1):129. DOI:10.1186/1742-2094-10-129 · 5.41 Impact Factor
Available from: S.P. Li
- "The major bioactive compounds in He-Shou-Wu have been reported to be stilibene and polyphenols. These compounds have multiple effects, such as antioxidation
[2,3], radical scavenging activity
, lipid regulation
[5,6], hair growing effect of resting hair follicles
, inhibition of advanced glycation end product formation
 and neuroprotection
[9-13]. Therefore, analysis of these compounds will be helpful to control the quality of Polygonum multiflorum. "
[Show abstract] [Hide abstract]
Polygoni Multiflori Radix, He-Shou-Wu in Chinese, is a widely used traditional Chinese medicine. Clinically, water decoction is the major application form of He-Shou-Wu. Therefore, simultaneous determination of bioactive compounds in water extract is very important for its quality control.
A pressurized liquid extraction and short-end injection micellar electrokinetic chromatography (MEKC) were first developed for simultaneous determination of seven hydrophilic bioactive compounds in water extract of He-Shou-Wu. The influence of parameters, such as pH, concentration of phosphate, SDS and HP-β-CD, capillary temperature and applied voltage, on the analysis were carefully investigated. Optimum separation was obtained within 14 min by using 50 mM phosphate buffer containing 90 mM SDS and 2% (m/v) HP-β-CD (pH 2.5) at 15 kV and 20°C. All calibration curves showed good linearity (R2>0.9978) within test ranges. The overall LOD and LOQ were lower than 2.0 μg/mL and 5.5 μg/mL, respectively. The RSDs for intra- and inter-day of seven analytes were less than 3.2% and 4.6%, and the recoveries were 97.0%-104.2%.
The validated method was successfully applied to the analysis of He-Shou-Wu samples, which is helpful for its quality control.
Chemistry Central Journal 03/2013; 7(1):45. DOI:10.1186/1752-153X-7-45 · 2.19 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: 1. 2,3,4′,5-Tetrahydroxystilbene-2-O-β-d-glucoside (TSG) has been shown to have an anti-atherosclerotic effect. Vascular smooth muscle cell (VSMC) proliferation contributes to the pathobiology of atherosclerosis. The aim of the present study was to investigate the effects of TSG on platelet-derived growth factor (PDGF)-BB-induced VSMC proliferation and to explore the molecular mechanisms underlying the effects.
2. Cultured rat VSMC were pretreated with TSG (l–50 μmol/L) for 1 h, followed by exposure to PDGF-BB (10 ng/mL) for 24 h, after which cell proliferation and cell cycle stages were examined. The expression of protein cell cycle regulators, including retinoblastoma (Rb), cyclin D1/E, cyclin-dependent kinase (CDK) 2/4, CDK inhibitors p21 and p27 and proliferative cell nuclear antigen (PCNA), was examined. Activation of extracellular signal-regulated kinase (ERK) 1/2 was evaluated to elucidate the possible upstream mechanism by which TSG affects cell cycle regulators.
3. The results showed that TSG dose-dependently inhibited PDGF-BB-induced VSMC proliferation, possibly by blocking the progression of the cell cycle from the G1 to S phase. In addition, TSG significantly inhibited PDGF-BB-induced phosphorylation of Rb and the expression of cyclin D1, CDK4, cyclin E, CDK2 and PCNA. In addition, TSG suppressed PDGF-BB-induced downregulation of p27 and upregulation of p21, as well as PDGF-BB-induced activation of ERK1/2.
4. Together, the findings of the present study provide the first evidence that TSG can inhibit PDGF-BB-stimulated VSMC proliferation via cell cycle arrest in association with modulation of the expression of cell cycle regulators, which may be mediated, at least in part, by suppression of ERK1/2 activation.
Clinical and Experimental Pharmacology and Physiology 02/2011; 38(5):307-13. DOI:10.1111/j.1440-1681.2011.05502.x · 2.37 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.