• Journal of Ginseng Research
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• v.5 no.1
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• pp.41-48
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• 1981

Total saponin, protopanaxadiol-saponin and protopanaxatriol-saponin were isolated and purified from the side roots of red ginseng. After we administered them orally into rats during 5 weeks, we observed their effects on lipid and glucose content in rat serum. The change in body weight of protopanaxatriol- saponin treated group was slightly larger than those of other groups. Total lipid content in total saponin treated group showed an increase of about 20 % over that in control group. However, protopanaxadiol-saponin and protopanaxatriol- saponin treated groups showed no change. While triglyceride content in total saponin treated group decreased 29oyo compared to it s content in control group, its content in protopanaxatriol-saponin treated group increased 45%. Three saponin treated groups showed lower value than control group in total ant free cholesterol levels. While glucose content in total saponin treated group decreased slightly, that in Protopanaxadiol-saponin treated group decreased slightly compared to that in control group. And protopanaxatriol- saponin trented group showed the significant decrease of 25%. From these results, it is supposed that total saponin accelerates the conversion of lipid into glucose and that protopanaxatriol- saponin accelerates the conversion of glucose into lipid.

• Korean Journal of Pharmacognosy
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• v.26 no.4
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• pp.360-367
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• 1995

The metabolism of ginseng saponins by human intestinal bacteria was studied using human feces under anaerobic culture conditions. $Ginsenoside-Rb_1$, $-Rb_2$ and -Rc(protopanaxadiol type) were mainly metabolized to compound-K(C-K), $20-O-[{\alpha}-L-arabinopyranosyl(1{\rightarrow}6)-{\beta}-{_D}-glucopyranosyl]-20(S)-protopanaxadiol(compound-Y,\;C-Y)$, $20-O-[{\alpha}-L-arabinopyranosyl(1{\rightarrow}6)-{\beta}-{_D}-glucopyranosyll-20(S)-protopanaxadiol(ginsenosied-MC,{\;}MC)$, respectively, and $ginsenoside-Rg_1$ and -Re(protopanaxatriol type) to their aglycon, 20(S)-protopanaxatriol, though the pathway and rate of the metabolism were affected by fermentation medium. C-K was not decomposed any more, while C-Y and Mc were both gradually hydrolyzed to C-K.

• Journal of Ginseng Research
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• v.39 no.3
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• pp.189-198
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• 2015

Background: Antiallergic effect of 20(S)-protopanaxatriol (PPT), an intestinal metabolite of ginseng saponins, was investigated in guinea pig lung mast cells and mouse bone marrow-derived mast cells activated by a specific antigen/antibody reaction. Methods: Increasing concentrations of PPT were pretreated 5 min prior to antigen stimulation, and various inflammatory mediator releases and their relevant cellular signaling events were measured in those cells. Results: PPT dose-dependently reduced the release of histamine and leukotrienes in both types of mast cells. Especially, in activated bone marrow-derived mast cells, PPT inhibited the expression of Syk protein, cytokine mRNA, cyclooxygenase-1/2, and phospholipase $A_2$ ($PLA_2$), as well as the activities of various protein kinase C isoforms, mitogen-activated protein kinases, $PLA_2$, and transcription factors (nuclear factor-${\kappa}B$ and activator protein-1). Conclusion: PPT reduces the release of inflammatory mediators via inhibiting multiple cellular signaling pathways comprising the $Ca^{2+}$ influx, protein kinase C, and $PLA_2$, which are propagated by Syk activation upon allergic stimulation of mast cells.

• Korean Journal of Pharmacognosy
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• v.28 no.1
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• pp.35-41
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• 1997

Following ginsenoside-Rb1-hydrolyzing assay, strictly anaerobic bacteria were isolated from human feces and identified as Prevotella oris. The bacteria hydrolyzed ginsenoside Rb1 and Rd to $20-O-{\beta}-D-glucopyranosyl-20(S)-protopanaxadiol$ (I), ginsenoside Rb2 to $20-O-[{\alpha}-L-arabinofuranosyl (1{\rightarrow}6)-{\beta}-D-glucopyranosyl] - 20(S)-protopanaxadiol$ (ll) and ginsenoside Rc to $20-O-[{\alpha}-L-arabinofuranosyl (1{\rightarrow} 6){\beta}-D-g1ucopyranosyl]-20(S)-protopanaxadiol$ (III) like fecal microflora, but did not attack ginsenoside Re nor Rgl (Protopanaxatriol-type). Pharmacokinetic studies of ginseng saponins was also performed using specific pathogen free rats and demonstrated that the intestinal bacterial metabolites I-111, 20(S)- protopanaxatriol(IV) and 20(S)-protopanaxadiol(V) were absorbed from the intestines to $blood(0.4-5.1\;{\mu}g/ml)$ after oral administration with total saponin(1 g/kg/day).

• Journal of Microbiology and Biotechnology
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• v.27 no.9
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• pp.1559-1565
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• 2017

Naturally occurring ginsenoside F1 (20-O-${\beta}$-$\text\tiny{D}$-glucopyranosyl-20(S)-protopanaxatriol) is rare. Here, we produced gram-scale quantities of ginsenoside F1 from a crude protopanaxatriol saponin mixture comprised mainly of Re and Rg1 through enzyme-mediated biotransformation using recombinant ${\beta}$-glucosidase (BgpA) cloned from a soil bacterium, Terrabacter ginsenosidimutans Gsoil $3082^T$. In a systematic step-by-step process, the concentrations of substrate, enzyme, and NaCl were determined for maximal production of F1. At an optimized NaCl concentration of 200 mM, the protopanaxatriol saponin mixture (25 mg/ml) was incubated with recombinant BgpA (20 mg/ml) for 3 days in a 2.4 L reaction. Following octadecylsilyl silica gel column chromatography, 9.6 g of F1 was obtained from 60 g of substrate mixture at 95% purity, as assessed by chromatography. These results represent the first report of gram-scale F1 production via recombinant enzyme-mediated biotransformation.

• Journal of Ginseng Research
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• v.20 no.1
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• pp.111-112
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• 1996

The chemical shifts of C-21 and C-23 in the $^{13}C$-NMR for (20R)-protopanaxatriol, (20R)-ginsenoside $Rh_1$ and (20R)-ginsenoside $Rg_3$ were revised by employing some extensive 2D-NMR techniques.

• Journal of Ginseng Research
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• v.44 no.5
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• pp.690-696
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• 2020

Background: As the main metabolites of ginsenosides, 20(S, R)-protopanaxadiol [PPD(S, R)] and 20(S, R)-protopanaxatriol [PPT(S, R)] are the structural basis response to a series of pharmacological effects of their parent components. Although the estrogenicity of several ginsenosides has been confirmed, however, the underlying mechanisms of their estrogenic effects are still largely unclear. In this work, PPD(S, R) and PPT(S, R) were assessed for their ability to bind and activate human estrogen receptor α (hERα) by a combination of in vitro and in silico analysis. Methods: The recombinant hERα ligand-binding domain (hERα-LBD) was expressed in E. coli strain. The direct binding interactions of ginsenosides with hERα-LBD and their ERα agonistic potency were investigated by fluorescence polarization and reporter gene assays, respectively. Then, molecular dynamics simulations were carried out to simulate the binding modes between ginsenosides and hERα-LBD to reveal the structural basis for their agonist activities toward receptor. Results: Fluorescence polarization assay revealed that PPD(S, R) and PPT(S, R) could bind to hERα-LBD with moderate affinities. In the dual luciferase reporter assay using transiently transfected MCF-7 cells, PPD(S, R) and PPT(S, R) acted as agonists of hERα. Molecular docking results showed that these ginsenosides adopted an agonist conformation in the flexible hydrophobic ligand-binding pocket. The stereostructure of C-20 hydroxyl group and the presence of C-6 hydroxyl group exerted significant influence on the hydrogen bond network and steric hindrance, respectively. Conclusion: This work may provide insight into the chemical and pharmacological screening of novel therapeutic agents from ginsenosides.

• Journal of Ginseng Research
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• v.33 no.4
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• pp.316-323
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• 2009

Ginseng saponins have various pharmacological effects on the immune system. 20(S)-protopanaxadiol (PPD) and 20(S)-protopanaxatriol (PPT) are the species of ginseng saponin metabolites that are formed by human intestinal bacteria and detected in circulation. The effects of PPD and PPT on the inflammatory mediator release from the activated mast cells were tested. Histamine release was evaluated in activated guinea pig lung mast cells, and the secretion of interleukin-4 (IL-4), interleukin-8 (IL-8), and the tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) was assessed in an HMC-1 cell after treating it with ginseng saponin metabolites. The results are as follows. PPT, at its maximum concentration of $100\;{\mu}M$, completely abolished the secretion of IL-4 from the PMA-stimulated HMC-1 cell. It also inhibited IL-8 secretion from the same cells by about 40-50% of the PMA-treated DMSO control. PPD, at its maximum concentration of $100\;{\mu}M$, showed a tendency to induce histamine release from the guinea pig lung mast cells. It inhibited the secretion of IL-4 (by 89% of the PMA-treated DMSO control) in the PMA-stimulated HMC-1 cell, but did have a significant effect on the IL-8 release from the same cell. Both PPD and PPT showed no effects, however, on the release of TNF-${\alpha}$ from the PMA-stimulated HMC-1 cell. These results suggest that PPD and PPT are from the ginseng metabolites that are responsible for the immunomodulating activity of ginseng extracts when they are taken orally.

• Archives of Pharmacal Research
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• v.7 no.1
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• pp.17-22
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• 1984

Effects of total ginseng saponin, 20-S-protopanaxadiol saponin, 20-S-protopanaxatriol saponin and playcodon saponin on the osmotic behavior of liposomes were investigated by optical measurement. These saponins showed different activities on liposomal membrane, and cholesterol in liposomes was an important factor to this variation of saponin activities.

• Journal of Life Science
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• v.26 no.12
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• pp.1422-1430
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• 2016

This study was performed to investigate the modulatory effects of two prototypes of Panax ginseng saponin fractions, 20(S)-protopanaxadiol saponins (PDS) and 20(S)-protopanaxatriol saponins (PTS), on the induction of inflammatory mediators in lipopolysaccharide (LPS)-treated RAW264.7 murine macrophage cells. For this purpose, RAW264.7 cells were treated with LPS ($10{\mu}g/ml$) before, after, or simultaneously with PDS or PTS ($150{\mu}g/ml$), and the released level of nitric oxide (NO) and expression levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were evaluated. When RAW264.7 cells were treated with LPS and ginseng saponin fractions simultaneously for 24 hr, PTS, compared to PDS, more strongly attenuated the NO production induced by LPS treatment. When the cells were pretreated with LPS for 2 hr followed by PDS or PTS treatment for 24 hr, both ginseng saponins strongly reduced NO release. The pretreatment of RAW264.7 cells with PDS or PTS for 2 hr followed by LPS treatment for 24 hr significantly attenuated the LPS-induced production of NO. PTS showed stronger inhibitory potency to NO generation than PDS. Our western blot experiment showed that both PDS and PTS ($150{\mu}g/ml$) also significantly down-regulated the expressions of iNOS and COX-2 induced by LPS treatment. Our results suggest that both PDS and PTS possess strong protective effects against LPS-stimulated inflammation and that their protective effects are mediated by the suppression of NO synthesis via down-regulation of pro-inflammatory enzymes, iNOS, and COX-2 in the RAW264.7 cells.