• Journal of Ginseng Research
• /
• v.27 no.3
• /
• pp.129-134
• /
• 2003

When ginsenoside $R_{*}$b1/ and $R_{b2}$ were anaerobically incubated with human fecal microflora, these ginsenosides were metabolized to compound K (IH-901). When ginsenoside $R_{g3}$ was anaerobically incubated with human fecal microflora, the ginsenoside $R_{g3}$ was metabolized it to ginsenoside $R_{h2}$. Among ginsenosides, IH-901 and 20(S)-ginsenoside $R_{h2}$ exhibited the most potent cyotoxicity against tumor cells: 50% cytotoxic concentrations of IH-901 in the media with and without fetal bovine serum (FBS) were 27.1-31.6 $\mu$M and 0.1-0.61 $\mu$M, and those of 20(S)-ginsenoside $R_{h2}$ were 37.5->50 and 0.7-7.1 $\mu$M, respectively. The cytotoxic potency of ginsenosides was IH-901>20(S)-ginsenoside R $h_{h2}$》20(S)-ginsenoside $R_{g3}$>ginsenoside $R_{b1}$(equation omitted) $R_{b2}$.EX>$R_{b2}$./.

• Archives of Pharmacal Research
• /
• v.26 no.1
• /
• pp.58-63
• /
• 2003

Ginseng has been recommended to alleviate the menopausal symptoms, which indicates that components of ginseng very likely contain estrogenic activity. We have examined the possibility that a component of Panax ginseng, $ginsenoside-R_{b1}$ acts by binding to estrogen receptor. We have investigated the estrogenic activity of $ginsenoside-R_{b1}$ in a transient transfection system using estrogen-responsive luciferase plasmids in MCF-7 cells. $ginsenoside-R_{b1}$ activated the transcription of the estrogen-responsive luciferase reporter gene in MCF-7 breast cancer cells at a concentration of 50 $\mu$M. Activation was inhibited by the specific estrogen receptor antagonist ICI 182,780, indicating that the estrogenic effect of $ginsenoside-R_{b1}$ is estrogen receptor dependent. Next, we evaluated the ability of $ginsenoside-R_{b1}$ to induce the estrogen-responsive gene c-fos by semi-quantitative RT-PCR assays and Western analyses. $ginsenoside-R_{b1}$ increased c-fos both at mRNA and protein levels. However, $ginsenoside-R_{b1}$ failed to activate the glucocorticoid receptor, the retinoic acid receptor, or the androgen receptor in CV-1 cells transiently transfected with the corresponding steroid hormone receptors and hormone responsive reporter plasmids. These data support our hypothesis that $ginsenoside-R_{b1}$ acts a weak phytoestrogen, presumably by binding and activating the estrogen receptor.

• Proceedings of the PSK Conference
• /
• 2003.10b
• /
• pp.160.2-160.2
• /
• 2003

When ginsenoside $R_{b1}$ and $R_{b2}$ were anaerobically incubated with human fecal microflora, these ginsenosides were metabolized to compound K. When ginsenoside $R_{g3}$ was anaerobically incubated with human fecal microflora, the ginsenoside $R_{g3}$ was metabolized it to ginsenoside $R_{h2}$. Among ginsenosides, compound K and 20(S)-ginsenoside $R_h2$ exhibited the most potent cyotoxicity against tumor cells: 50% cytotoxic concentrations of compound K in the media with and without fetal bovine serum (FBS) were 27.1 - 31.6 mM and0.1 - 0.6 mM, and those of 20(S)-ginsenoside $R_h2$ were 37.5 $\rightarrow$ 50 and 0.7 - 7.1 mM mM, respectively. (omitted)

• Microbiology and Biotechnology Letters
• /
• v.17 no.2
• /
• pp.126-130
• /
• 1989

In 14 kinds of ginsenosides in ginseng saponin, ginsenoside Rbr is contained the most abundantly. But ginsenoside Rd which is similar to ginsenoside R $b_1$in structure, was known to be superior to ginsenoside R $b_1$pharmaceutically. The convertible enzyme which can transform ginsenoside R $b_1$to Binsenoside Rd specifically among ginseng saponin, was purified homogeneously from Rhizopus japonicus. The optimal pH for the action of the enzyme was pH 4.8 to 5.0, and optimal temperature was 45$^{\circ}C$. The enzyme was stable in the range of pH 4.0 to 9.0, and the half activity of enzyme was remained by the thermal treatment at 6$0^{\circ}C$ for 2 hours. The enzyme activity was enhanced by addition of M $n^{++}$ or Fe, though inhibited by EDTA or o-phenanthroline. On the substrate specificity, the enzyme was. able to hydrolyze gentiobiose, cellobiose, amygdalin and prunasin, but not to hydrolyze any other kinds of Binsenosides besides Binsenoside R $b_1$. Km values of the enzyme for ginsenoside R $b_1$, gentiobiose and amygdalin were 5.0mM, 4.8mM and 3.7mM, respectively.3.7mM, respectively.y.

• Applied Biological Chemistry
• /
• v.25 no.4
• /
• pp.211-217
• /
• 1982

Ginsenosides in epidermis·cortex(EC) and xylem-pith(XP) of main body of Panax ginseng(var. atropurpureacaulo) root were investigated in relation to dark purple area on stem. Pattern of ginsenosides, ratio of protopanaxatriol(PT) to diol(PD) and total ginsenoside content were significantly different between EC ana XP, and not related with stem color. The increasing trend of total ginsenosides with decreasing in purple area on stem needs to be tested with greater sample size. The order of ginsenoside content was $Rb_1>Rg_1>Re>Rc>Rg_2>Rb_2>Rf>Rd$ for EC, $Rg_1>Rb_1>Rg_2>Re>Rb_2>Rc>Rf>Rd$ for XP. PT/PD was 1.08 for EC,1.95 for XP. Since total ginsenoside content was 3 times higher in EC than in XP and weight of two parts was almost same, the content of ginsenosides of main body mostly depends on those of EC.

• Journal of Ginseng Research
• /
• v.47 no.2
• /
• pp.274-282
• /
• 2023

Background: Ginsenoside compound K (CK) stimulated activation of the PI3K-Akt signaling is one of the major mechanisms in promoting cell survival after stroke. However, the underlying mediators remain poorly understood. This study aimed to explore the docking protein of ginsenoside CK mediating the neuroprotective effects. Materials and methods: Molecular docking, surface plasmon resonance, and cellular thermal shift assay were performed to explore ginsenoside CK interacting proteins. Neuroscreen-1 cells and middle cerebral artery occlusion (MCAO) model in rats were utilized as in-vitro and in-vivo models. Results: Ginsenoside CK interacted with recombinant human PTP1B protein and impaired its tyrosine phosphatase activity. Pathway and process enrichment analysis confirmed the involvement of PTP1B and its interacting proteins in PI3K-Akt signaling pathway. PTP1B overexpression reduced the tyrosine phosphorylation of insulin receptor substrate 1 (IRS1) after oxygen-glucose deprivation/reoxygenation (OGD/R) in neuroscreen-1 cells. These regulations were confirmed in the ipsilateral ischemic hemisphere of the rat brains after MCAO/R. Ginsenoside CK treatment reversed these alterations and attenuated neuronal apoptosis. Conclusion: Ginsenoside CK binds to PTP1B with a high affinity and inhibits PTP1B-mediated IRS1 tyrosine dephosphorylation. This novel mechanism helps explain the role of ginsenoside CK in activating the neuronal protective PI3K-Akt signaling pathway after ischemia-reperfusion injury.

• Proceedings of the Ginseng society Conference
• /
• 1978.09a
• /
• pp.55-66
• /
• 1978

Five ginsenosides $(A_1,\;A_2,\;B_1,\;B_2,\;C)$ and a yellow pigment were isolated from American ginseng stems and leaves. Ginsenoside $A_2,\;B_1,\;B_2$ and C were proven to be identical with Korean ginseng root ginsenoside $Rg_1,$ Rd, Re and $Rb_2,$ respectively. The yellow pigment proved identical with panasenoside isolated from Korean ginseng leaves. Ginsenoside $A_1$, which was also present in American ginseng roots, was not identical to any of the known root (ginsenoside $R_{0}-Rg_{2}$) and leaf (ginsenoside $F_{1}-F_{3}$) Korean ginseng saponins. A gas-liquid chromatographic method was developed to analyze ginsenosides and sapogenins in rabbit plasma and urine samples. Panasenoside and stigmasterol were found to be the best internal standards for ginsenosides and sapogenihs, respectively. Ginsenoside C had a significantly longer half-life, higher plasma protein binding, lower metabolic and renal clearance than ginsenoside $A_1,\;A_2\;and\;B_2$. Ginsenosides were not found in rabbit plasma and urine samples after oral administration. Ginsenoside C had a higher toxicity than ginsenoside $A_2$ after intraperitoneal administration to mice. Toxicity was not observed after oral administration of the ginsenosides.

• Journal of Ginseng Research
• /
• v.44 no.2
• /
• pp.274-281
• /
• 2020

Background: Ultraviolet (UV) goes through the epidermis and promotes release of inflammatory cytokines in keratinocytes. Granulocyte-macrophage colony-stimulating factor (GM-CSF), one of the keratinocyte-derived cytokines, regulates proliferation and differentiation of melanocytes. Extracellular signal-regulated kinase (ERK1/2) and protein kinase C (PKC) signaling pathways regulate expression of GM-CSF. Based on these results, we found that ginsenoside Rh3 prevented GM-CSF production and release in UV-B-exposed SP-1 keratinocytes and that this inhibitory effect resulted from the reduction of PKCδ and ERK phosphorylation. Methods: We investigated the mechanism by which ginsenoside Rh3 from Panax ginseng inhibited GM-CSF release from UV-B-irradiated keratinocytes. Results: Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) or UV-B induced release of GM-CSF in the SP-1 keratinocytes. To elucidate whether the change in GM-CSF expression could be related to PKC signaling, the cells were pretreated with H7, an inhibitor of PKC, and irradiated with UV-B. GM-CSF was decreased by H7 in a dose-dependent manner. When we analyzed which ginsenosides repressed GM-CSF expression among 15 ginsenosides, ginsenoside Rh3 showed the largest decline to 40% of GM-CSF expression in enzyme-linked immunosorbent assay. Western blot analysis showed that TPA enhanced the phosphorylation of PKCδ and ERK in the keratinocytes. When we examined the effect of ginsenoside Rh3, we identified that ginsenoside Rh3 inhibited the TPA-induced phosphorylation levels of PKCδ and ERK. Conclusion: In summary, we found that ginsenoside Rh3 impeded UV-B-induced GM-CSF production through repression of PKCδ and ERK phosphorylation in SP-1 keratinocytes.

• Korean Journal of Plant Tissue Culture
• /
• v.27 no.6
• /
• pp.461-468
• /
• 2000

For the enhancement of ginsenoside production in hairy roots cultures of Panax ginseng, the uptake rate of inorganic elements and ginsenoside contents were investigated by different concentrations of about phosphorus (P $O_{4}$$^{[-10]}$ ) and nitrogen (N $H_{4}$$^{+}$, N $O_{3}$$^{[-10]}$ ) sources. According to increased phosphorus and nitrogen sources, the uptake rate of $Mg^{2+}$ and F $e^{2+}$ in ginseng hairy roots were significantly increased. The uptake rate of F $e^{2+}$ in 5.15 mM N $H_{4}$$^{+}$ was higher at 47.5% than that in 20.6 mM, whereas that of C $u^{2+}$ in 10.3 mM were higher at 123.1% than that in 41.2 mM. These results indicated that phosphorus and nitrogen sources act not only elevated growth of hairy roots but also the uptake-enhancement of the irons and other ions. The optimum concentration of phosphorus and nitrogen sources for the contents of free sugars were different to kinds of free sugars. The optimum concentration of phosphorus and nitrogen sources for the ginsenoside formation in ginseng hairy roots cultures were highest at the most low concentration of all. The contents of ginsenoside-R $b_2$and -Rc in 0.31 mM P $O_{4}$$^{[-10]}$ were increased to 44.7% and 29.9% than that in 0.62 mM P $O_{4}$$^{[-10]}$ , respectively. The contents of ginsenoside-R $b_2$ and -Rc in 5.15 mM N $H_{4}$$^{+}$ were increased to 21.7% and 31.9% than that in 10.30 mM N $H_{4}$$^{+}$, respectively. The contents of ginsenoside-R $b_2$and -Rc in 4.7 mn N $O_{3}$$^{[-10]}$ were also increased to 17.6% and 25.5% than that in 9.4 mM N $O_{3}$$^{[-10]}$ , respectively. These results indicate that enhancement of the ginsenoside formation in ginseng hairy roots was feasible by new medium modulation of concentration of phosphorus and nitrogen sources.rogen sources.

• Journal of Ginseng Research
• /
• v.46 no.3
• /
• pp.376-386
• /
• 2022

Background: Brain-derived neurotrophic factor (BDNF)-tropomyosin-related kinase B (TrkB) plays a critical role in the pathogenesis of depression by modulating synaptic structural remodeling and functional transmission. Previously, we have demonstrated that the ginsenoside Rb1 (Rb1) presents a novel antidepressant-like effect via BDNF-TrkB signaling in the hippocampus of chronic unpredictable mild stress (CUMS)-exposed mice. However, the underlying mechanism through which Rb1 counteracts stress-induced aberrant hippocampal synaptic plasticity via BDNF-TrkB signaling remains elusive. Methods: We focused on hippocampal microRNAs (miRNAs) that could directly bind to BDNF and are regulated by Rb1 to explore the possible synaptic plasticity-dependent mechanism of Rb1, which affords protection against CUMS-induced depression-like effects. Results: Herein, we observed that brain-specific miRNA-134 (miR-134) could directly bind to BDNF 30 UTR and was markedly downregulated by Rb1 in the hippocampus of CUMS-exposed mice. Furthermore, the hippocampus-targeted miR-134 overexpression substantially blocked the antidepressant-like effects of Rb1 during behavioral tests, attenuating the effects on neuronal nuclei-immunoreactive neurons, the density of dendritic spines, synaptic ultrastructure, long-term potentiation, and expression of synapse-associated proteins and BDNF-TrkB signaling proteins in the hippocampus of CUMS-exposed mice. Conclusion: These data provide strong evidence that Rb1 rescued CUMS-induced depression-like effects by modulating hippocampal synaptic plasticity via the miR-134-mediated BDNF signaling pathway.