Dataset Information

Biological Effects of Tetrahydroxystilbene Glucoside: An Active Component of a Rhizome Extracted from Polygonum multiflorum.

ABSTRACT: Polygonum multiflorum Thunb. (PM), a traditional Chinese medicinal herb, has been widely used in the Orient as a tonic and antiaging agent. 2,3,5,4'-Tetrahydroxystilbene-2-O-?-D-glucoside (TSG, C20H22O9, FW?=?406.38928) is one of the active components extracted from PM. TSG is an antioxidant agent, which exhibits remarkable antioxidative activities in vivo and in vitro. The antioxidant effect of TSG is achieved by its radical-scavenging effects. TSG can inhibit apoptosis and protect neuronal cells against injury through multifunctional cytoprotective pathways. TSG performs prophylactic and therapeutic activities against Alzheimer's disease, Parkinson's disease, and cerebral ischemia/reperfusion injury. It is also antiatherosclerotic and anti-inflammatory. However, the mechanisms underlying these pharmacological activities are unclear. This study aimed at reviewing experimental studies and describing the effectiveness and possible mechanisms of TSG.

SUBMITTER: Zhang L

PROVIDER: S-EPMC6247474 | biostudies-other | 2018

REPOSITORIES: biostudies-other

ACCESS DATA

Publications

Biological Effects of Tetrahydroxystilbene Glucoside: An Active Component of a Rhizome Extracted from Polygonum multiflorum.

Zhang Lingling L Chen Jianzong J

Oxidative medicine and cellular longevity 20181104

Polygonum multiflorum Thunb. (PM), a traditional Chinese medicinal herb, has been widely used in the Orient as a tonic and antiaging agent. 2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-glucoside (TSG, C20H22O9, FW = 406.38928) is one of the active components extracted from PM. TSG is an antioxidant agent, which exhibits remarkable antioxidative activities in vivo and in vitro. The antioxidant effect of TSG is achieved by its radical-scavenging effec ...[more]

PMID: 30524653

Similar Datasets

Project description:The clinical use of Polygonum multiflorum Thunb (PM) has been restricted or banned in many countries, due to its hepatotoxic adverse effects. Its toxicity research has become a hot topic. So far, the pharmacokinetic studies of PM, focusing on prototype compounds such as 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), emodin, and physcion, have been considered the main basis of pharmacodynamic material or of toxic effect. However, pharmacokinetic studies of its phase II metabolites have not yet been reported, mainly because the quantifications of such metabolites are difficult to do without the reference substance. In addition, pharmacokinetic studies on different pathological models treated with PM have also not been reported. On the other hand, toxic effects of PM have been reported in patients diagnosed with different liver pathologies. In the present work, a simultaneous quantitation method for eight prototypes components of PM and their five phase II metabolites has been performed by ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) and used for the pharmacokinetic study of PM in two different liver pathological models in rats (normal, alpha-naphthylisothiocyanate (ANIT), and carbon tetrachloride (CCl4)). The results showed that the main blood-entering components of PM are TSG, emodin, physcion, emodin-8-O-β⁃D⁃glucoside (E-Glu), physcion-8-O-β⁃D⁃glucoside (P-Glu), aloe-emodin, gallic acid, resveratrol and catechin, among which TSG, emodin, and catechin were primary metabolized in phase II, while resveratrol was converted to all phase II metabolites, and the others were metabolized as drug prototypes. Meanwhile, their pharmacokinetic parameters in the different models also exhibited significant differences. For instance, the AUC (0-∞) values of the TSG prototype and its phase II metabolites were higher in the ANIT group, followed by CCl4 group and the normal group, while the AUC (0-∞) values of the emodin prototype and its phase II metabolites were higher in the CCl4 group. To further illustrate the reasons for the pharmacokinetic differences, bilirubin metabolizing enzymes and transporters in the liver were measured, and the correlations with the AUC of the main compounds were analyzed. TSG and aloe-emodin have significant negative correlations with UGT1A1, BSEP, OATP1A4, OCT1, NTCP, MRP2 and MDR1 (p < 0.01). These data suggest that when the expression of metabolic enzymes and transporters in the liver is inhibited, the exposure levels of some components of PM might be promoted in vivo.

Project description:BackgroundThe idiosyncratic hepatotoxicity of Polygonum multiflorum (PM) has attracted considerable interest, but the idiosyncratically hepatotoxic components and endogenous metabolite changes resulting from idiosyncratic hepatotoxicity of PM are not well understood. The aim of this study was to identify the idiosyncratically hepatotoxic components and potential endogenous metabolic biomarkers for PM-induced liver injury.MethodsSerum biochemical indicators and hematoxylin and eosin (H&E) staining were evaluated to identify pathological changes. Gas chromatography/mass spectrometry (GC-MS) was performed to identify changes in metabolic biomarkers. Orthogonal projection to latent structures discriminant analysis (OPLS-DA) was applied to determine group clustering trends and differential metabolites.ResultsThe results for the liver index, the liver function index and liver pathology showed that Polygonum multiflorum ethanol extract (PME), 50% ethanol elution fractions and tetrahydroxystilbene glucoside (TSG) from PME can induce idiosyncratic hepatotoxicity. TSG was the main idiosyncratically hepatotoxic component. Forty endogenous metabolites were identified in the rat liver. Six biomarkers, including lower levels of L-valine and higher levels of 3-hydroxybutyric acid, hexadecanoic acid, ribose, phosphoric acid and oxalic acid, were related to PM-induced liver injury. These differential biomarkers led to disruptions in amino acid, fatty acid, oxalate, energy and glucose metabolism. A total of 32 types of endogenous metabolites were identified in rat serum. Ten biomarkers were related to the liver injury induced by TSG, including lower levels of L-valine and L-proline and higher levels of urea, caproic acid, DL-malic acid, D-mannose, 3-hydroxybutyric acid, D-galactose, octadecane and hexadecanoic acid. These differential biomarkers led to disruptions in amino acid, glucose and fat metabolism. The mechanism of idiosyncratic hepatotoxicity in PM involves TSG-induced disruptions in amino acid metabolism, lipid metabolism, energy metabolism and glucose metabolism.ConclusionsThese findings reflect the material basis and metabolic mechanism of idiosyncratic PM hepatotoxicity.

Dataset Information

Biological Effects of Tetrahydroxystilbene Glucoside: An Active Component of a Rhizome Extracted from Polygonum multiflorum.

Publications

Biological Effects of Tetrahydroxystilbene Glucoside: An Active Component of a Rhizome Extracted from <i>Polygonum multiflorum</i>.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets