In vivo pharmacokinetic and metabolism studies of ginsenoside Rd

Liu, Yang; Deng, Yangdong; Xu, Shun-jun; Zeng, Xing

doi:10.1016/j.jchromb.2007.04.014

Cited by 80 publications

(44 citation statements)

References 17 publications

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“…No reports of ginsenosides glucuronidation were found in the literature. In a pharmacokinetic study in which ginsenoside Rd was administered intravenously to volunteers, no glucuronide conjugates were detected in plasma [76]. Another in vitro study on metabolism of ginsenoside Rg3 using rat S9 liver fraction did not detect any glucuronidated metabolites [77].…”

Section: Ginsengmentioning

confidence: 96%

Effects of Herbal Supplements on Drug Glucuronidation. Review of Clinical, Animal, andIn VitroStudies

Mohamed

Frye

2010

Planta Med

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Section: Ginsengmentioning

confidence: 96%

Effects of Herbal Supplements on Drug Glucuronidation. Review of Clinical, Animal, andIn VitroStudies

Mohamed

Frye

2010

Planta Med

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“…Ginsenoside Rd (GSRd, Fig. 1) is one of the major active components of ginsenosides (Nah et al 2007;Yang et al 2007a).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rd Protects Neurons Against Glutamate-Induced Excitotoxicity by Inhibiting Ca2+ Influx

Zhang

Shi

et al. 2011

Cell Mol Neurobiol

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Our previous studies have demonstrated that ginsenoside Rd (GSRd), one of the principal ingredients of Pana notoginseng, has neuroprotective effects against ischemic stroke. However, the possible mechanism(s) underlying the neuroprotection of GSRd is/are still largely unknown. In this study, we treated glutamate-injured cultured rat hippocampal neurons with different concentrations of GSRd, and then examined the changes in neuronal apoptosis and intracellular free Ca(2+) concentration. Our MTT assay showed that GSRd significantly increased the survival of neurons injured by glutamate in a dose-dependent manner. Consistently, TUNEL and Caspase-3 staining showed that GSRd attenuated glutamate-induced cell death. Furthermore, calcium imaging assay revealed that GSRd significantly attenuated the glutamate-induced increase of intracellular free Ca(2+) and also inhibited NMDA-triggered Ca(2+) influx. Thus, the present study demonstrates that GSRd protects the cultured hippocampal neurons against glutamate-induced excitotoxicity, and that this neuroprotective effect may result from the inhibitory effects of GSRd on Ca(2+) influx.

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“…10) However, several researchers reported that intact ginsenosides are only slightly absorbed through digestive tract, and the oral bioavailability of intact ginsenosides in the intestines is extremely low. [11][12][13][14] Ginsenosides act as precursors that are metabolized to the bioactive form by intestinal bacterial deglycosylation 15,16) and fatty acid esterification 17,18) in the body. Pharmacologic studies have shown the following metabolic pathways of ginsenosides in the human body: ginsenosides of the 20S-protopanaxadiol type are finally metabolized to 20S-protopanaxadiol 20-O-b-D-glucopyranoside (M 1 ), which is also called ginsenoside compound K; whereas ginsenosides of 20S-protopanaxatriol type are finally metabolized to 20S-protopanaxatriol (M 4 ) through cleavage of the oligosaccharides connected to the C-6 and C-20 hydroxyl groups of the aglycone by intestinal bacteria.…”

mentioning

confidence: 99%

Optimization of Ginsenosides Hydrolyzing .BETA.-Glucosidase Production from Aspergillus niger Using Response Surface Methodology

Zhu

Lee

et al. 2008

Biological & Pharmaceutical Bulletin

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To optimize ginsenosides hydrolyzing b b-glucosidase production from Aspergillus niger, response surface methodology was carried out in two stages. The Plackett-Burman design was achieved to screen the important variables that influence b b-glucosidase production. Among 10 variables (wheat bran, soybean powder, CaCl 2 , ginsenosides, KH 2 PO 4 , MgSO 4 , polyethylene glycol (PEG), medium volume, inoculum size, and stirring speed), it was found that wheat bran, KH 2 PO 4 , and stirring speed had significant effect on b b-glucosidase activity due to very low p-values (pϽ0.05). Subsequently, wheat bran, KH 2 PO 4 , and stirring speed were further optimized using central composite design. The optimal b b-glucosidase production was predicted to be 4650.14 U/ml with the combination of factors (wheat bran, 34.51 g/l; KH 2 PO 4 , 1.78 g/l; stirring speed, 161.60 rpm/min). Finally, under optimal fermentation conditions, ginsenoside Rb 1 was converted to Rd and F 2 by A. niger within 10 min. Little compound K was detected at 30 min, and finally F 2 was completely transformed to compound K within 8 h. The putative conversion pathway of Rb 1 by A. niger was Rb 1 , Rd, F 2 , and compound K.

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In vivo pharmacokinetic and metabolism studies of ginsenoside Rd

Cited by 80 publications

References 17 publications

Effects of Herbal Supplements on Drug Glucuronidation. Review of Clinical, Animal, andIn VitroStudies

Effects of Herbal Supplements on Drug Glucuronidation. Review of Clinical, Animal, andIn VitroStudies

Ginsenoside Rd Protects Neurons Against Glutamate-Induced Excitotoxicity by Inhibiting Ca2+ Influx

Optimization of Ginsenosides Hydrolyzing .BETA.-Glucosidase Production from Aspergillus niger Using Response Surface Methodology

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