Root Of Polygonum Cuspidatum Research Articles

Phytoestrogens from the roots of Polygonum cuspidatum (polygonaceae): structure-Requirement of hydroxyanthraquinones for estrogenic activity

The methanolic extract from the roots of Polygonum (P.) cuspidatum was found to enhance cell proliferation at 30 or 100μg/mL in MCF-7, an estrogen-sensitive cell line. By bioassay-guided separation from P. cuspidatum with the most potent activity, emodin and emodin 8-O-β-d-glucopyranoside were isolated as active principles. The methanolic extracts from Polygonum, Cassia, Aloe, and Rheum species, which were known to contain anthraquinones, also showed the MCF-7 proliferation. As a result of the evaluation of various anthraquinones from plant sources and synthetic anthraquinones, aloe-emodin, chrysophanol, chrysophanol 8-O-β-d-glucopyranoside, and 1,8-dihydroxyanthraquinone showed weak activity. On the other hand, alizalin and 2,6-dihydroxyanthraquinone as well as emodin having the 2- and/or 6-hydoxyl groups showed potent activity. These results show that the unchelated hydroxyl group is essential for strong activity. Emodin and 2,6-dihydroxyanthraquinone also inhibited 17β-estradiol binding to human estrogen receptors (ERs) with Ki values of 0.77 and 0.31μM for ERα and 1.5 and 0.69μM for ERβ. These findings indicate that hydroxyanthraquinones such as emodin are phytoestrogens with an affinity to human estrogen receptors.

Resveratrol Isolated from Polygonum cuspidatum Root Prevents Tumor Growth and Metastasis to Lung and Tumor-Induced Neovascularization in Lewis Lung Carcinoma-Bearing Mice

Resveratrol is a naturally occurring phytoalexine found in medicinal plants. We found that resveratrol, at doses of 2.5 and 10 mg/kg, significantly reduced the tumor volume (42%), tumor weight (44%) and metastasis to the lung (56%) in mice bearing highly metastatic Lewis lung carcinoma (LLC) tumors, but not at a dose of 0.6 mg/kg. Resveratrol did not affect the number of CD4(+), CD8(+) and natural killer (NK)1.1.(+) T cells in the spleen. Therefore, the inhibitory effects of resveratrol on tumor growth and lung metastasis could not be explained by natural killer or cytotoxic T-lymphocyte activation. In addition, resveratrol inhibited DNA synthesis most strongly in LLC cells; its 50% inhibitory concentration (IC(50)) was 6.8 micromol/L. Resveratrol at 100 micromol/L increased apoptosis to 20.6 +/- 1.35% from 12.1 +/- 0.36% (P < 0.05) in LLC cells, and decreased the S phase population to 22.1 +/- 1.03% and 29.2 +/- 0.27% from 35.2 +/- 1.72% (P < 0.05) at concentrations of 50 and 100 micromol/L, respectively. Resveratrol inhibited tumor-induced neovascularization at doses of 2.5 and 10 mg/kg in an in vivo model. Moreover, resveratrol significantly inhibited the formation of capillary-like tube formation from human umbilical vein endothelial cells (HUVEC) at concentrations of 10-100 micromol/L; the degree of the inhibition of capillary-like tube formation by resveratrol was 45.5% at 10 micromol/L, 50.2% at 50 micromol/L and 52.6% at 100 micromol/L. Resveratrol inhibited the binding of vascular endothelial growth factor (VEGF) to HUVEC at concentrations of 10-100 micromol/L, but not at concentrations of 1 and 5 micromol/L. The degree of inhibition of VEGF binding to HUVEC by resveratrol was 16.9% at 10 micromol/L, 53.2% at 50 micromol/L and 47.8% at 100 micromol/L. We suggest that the antitumor and antimetastatic activities of resveratrol might be due to the inhibition of DNA synthesis in LLC cells and the inhibition of LLC-induced neovascularization and tube formation (angiogensis) of HUVEC by resveratrol

Stilbene glycoside sulfates from Polygonum cuspidatum.

Ten naturally occurring stilbene glycoside sulfates (1-10) were isolated from an aqueous extract of the root of Polygonum cuspidatum. Their structures were established based on chemical evidence and spectroscopic techniques, including 2D NMR methods.

METHOD-DEPENDENT BIAS IN THE QUANTITATION OF CIS- AND TRANS-RESVERATROL GLUCOSIDES BY HIGH PERFORMANCE LIQUID CHROMATOGRAPHY

The concentrations of cis and trans-polydatin (resveratrol 3-β-glucoside) were measured in 133 red wines by two methods: Method A utilized normal phase HPLC with isocratic elution followed by UV detection, and Method B was based on reverse phase HPLC with gradient elution and photodiode array detection. In each method, 20 μL of sample was directly injected without prior treatment. For both polydatin isomers, Method B gave higher values. These discrepancies were more marked with the second of two Calibrators prepared by purification of trans-polydatin from the dried roots of Polygonum cuspidatum. Overall, the correlation coefficients for the two methods were only 0.442 and 0.704 for the cis and trans isomers, respectively. No explanation for these findings was forthcoming. These results demonstrate the need for caution in interpreting and comparing values for polydatins reported using different methods, and emphasize the need for pure synthetic standards of these compounds to allow valid inter-laboratory and inter-method comparisons.

Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) inhibits TNF-induced NF-kappaB activation, IkappaB degradation, and expression of cell surface adhesion proteins in human vascular endothelial cells.

Most inflammatory agents activate nuclear transcription factor-kappaB (NF-kappaB) which results in expression of genes for cytokines, adhesion molecules, and enzymes involved in amplification and perpetuation of inflammation. Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is an active component from the roots of Polygonum cuspidatum that has been reported to exhibit antiinflammatory properties but the mechanism is not known. In the present study we investigated the effects of emodin on the activation of NF-kappaB in human umbelical vein endothelial cells (EC). Treatment of EC with TNF activated NF-kappaB; preincubation with emodin inhibited this activation in a dose- and time-dependent manner. Emodin did not chemically modify NF-kappaB subunits but rather inhibited degradation of IkappaB, an inhibitory subunit of NF-kappaB. Since the promoter regions of ICAM-1, VCAM-1, and ELAM-1 contain NF-kappaB binding sites and these adhesion molecules are involved in the attachment of leukocytes to EC, the effect of emodin on the adhesion of monocytes to EC and the expression of these adhesion molecules was also studied. Treatment of EC with TNF for 6 h increased the adhesion of monocytes to EC, which correlated with increases in cell surface expression of ICAM-1, VCAM-1 and ELAM-1. Pretreatment of EC for 1 h with emodin inhibited both monocyte-EC attachment and expression of ICAM-1, ELAM-1 and VCAM-1. These results indicate that emodin is a potent inhibitor of NF-kappaB activation and expression of adhesion molecules and thus could be useful in treating various inflammatory diseases.

New Constitutents of Roots of Polygonum cuspidatum

A new naphtoquinone and 9 known phenolic components were isolated from a Japanese drug the roots of POLYGONUM CUSPIDATUM. The new component was proved to be 2-methoxy-6-acetyl-7-methyljuglone.

タデ科植物成分の研究 (第3報)

Dried root of Polygonum cuspidatum was consecutively extracted with ethanol and ether, transited to the alkaline solution, and submitted to liquid chromatography by which hydroxyanthraquinones were isolated. By repeated purification through vacuum sublimation and recrystallization, each was identified by zinc distillation, acetylation, or one-dimentional paper chromatography. Besides hydroxyanthraquinones, such as emodin, emodin monomethyl ether, and chrysophanic acid, some reddish brown amorphous powder of m.p. 280° (decomp.) was obtained and glucose and rhamnose were identified as their osazones. The total amount of hydroxyanthraquinoes was 0.1-0.5% of the dried root.