Ginsenoside Rh3

CAS# 105558-26-7

Ginsenoside Rh3

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Product Name & Size Price Stock
Ginsenoside Rh3:5mg $184.00 In stock
Ginsenoside Rh3:10mg $313.00 In stock
Ginsenoside Rh3:25mg $736.00 In stock
Ginsenoside Rh3:50mg $1288.00 In stock
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Quality Control of Ginsenoside Rh3

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Chemical structure

Ginsenoside Rh3

3D structure

Chemical Properties of Ginsenoside Rh3

Cas No. 105558-26-7 SDF Download SDF
PubChem ID 6439048 Appearance White powder
Formula C36H60O7 M.Wt 604.86
Type of Compound Triterpenoids Storage Desiccate at -20°C
Solubility Soluble ≥5 mg/ml in DMSO
Chemical Name (2R,3S,4S,5R,6R)-2-(hydroxymethyl)-6-[[(8R,10R,12S,13R,14S,17S)-12-hydroxy-4,4,8,10,14-pentamethyl-17-[(2Z)-6-methylhepta-2,5-dien-2-yl]-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]oxane-3,4,5-triol
SMILES CC(=CCC=C(C)C1CCC2(C1C(CC3C2(CCC4C3(CCC(C4(C)C)OC5C(C(C(C(O5)CO)O)O)O)C)C)O)C)C
Standard InChIKey PHLXREOMFNVWOH-WJJFPOJFSA-N
Standard InChI InChI=1S/C36H60O7/c1-20(2)10-9-11-21(3)22-12-16-36(8)28(22)23(38)18-26-34(6)15-14-27(33(4,5)25(34)13-17-35(26,36)7)43-32-31(41)30(40)29(39)24(19-37)42-32/h10-11,22-32,37-41H,9,12-19H2,1-8H3/b21-11-/t22-,23+,24-,25?,26?,27?,28+,29-,30+,31-,32+,34+,35-,36+/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Ginsenoside Rh3

The roots of Panax ginseng C. A. Mey.

Biological Activity of Ginsenoside Rh3

DescriptionGinsenoside Rh3 is a bacterial metabolite of Ginsenoside Rg5, Rh3 has anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways, it may improve chronic dermatitis or psoriasis by the regulation of IL-1β and TNF-α produced by macrophage cells and of IFN-γ produced by Th cells. Rg5 and Rh3 inhibited acetylcholinesterase activity in a dose-dependent manner, with IC50 values of 18.4 and 10.2 uM, respectively, they may protect memory deficit by inhibiting AChE activity and increasing BDNF expression and CREB activation.
TargetsCOX | IFN-γ | IL Receptor | TNF-α | cAMP | PKC | NOS | HO-1 | PI3K | Akt | JAK | STAT | AMPK | NF-kB | Nrf2
In vitro

Ginsenoside Rh2 and Rh3 induce differentiation of HL-60 cells into granulocytes: modulation of protein kinase C isoforms during differentiation by ginsenoside Rh2.[Pubmed: 9611775]

Int J Biochem Cell Biol. 1998 Mar;30(3):327-38.

Ginsenoside Rh3 and Rh4 were recently isolated from Panax ginseng, but their biochemical and pharmacological effects remain unidentified.
METHODS AND RESULTS:
The present study investigated whether the ginsenoside Rh group (G-Rh1, -Rh2, -Rh3 and -Rh4) having similar structures induce differentiation of HL-60 cells and whether protein kinase C (PKC) is involved in differentiation by ginsenoside. Differentiation was assessed by Wright-Giemsa stain and nitroblue tetrazolium reduction. G-Rh2 and Ginsenoside Rh3 induced differentiation of HL-60 cells into morphologically and functionally granulocytes but G-Rh1 and G-Rh4 did not. G-Rh2 and Ginsenoside Rh3 arrested the cell cycle at the G1/S phase, consistent with the ability to induce differentiation in a decreasing order of retinoic acid > G-Rh2 > Ginsenoside Rh3.
CONCLUSIONS:
It is concluded that G-Rh2 and Ginsenoside Rh3 can induce differentiation of HL-60 cells into granulocytes and modulation of PKC isoform levels may contribute to differentiation of HL-60 cells by G-Rh2.

In vivo

Inhibitory effect of ginsenoside Rg5 and its metabolite ginsenoside Rh3 in an oxazolone-induced mouse chronic dermatitis model.[Pubmed: 16964764]

Arch Pharm Res. 2006 Aug;29(8):685-90.

The effect of a main constituent ginsenoside Rg5 isolated from red ginseng and its metabolite Ginsenoside Rh3 in a chronic dermatitis model was investigated.
METHODS AND RESULTS:
Ginsenosides Rg5 and Rh3 suppressed swelling of oxazolone-induced mouse ear contact dermatitis. These ginsenosides also reduced mRNA expressions of cyclooxygenase-2, interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. The inhibition of Ginsenoside Rh3 was more potent than that of ginsenoside Rg5.
CONCLUSIONS:
These findings suggest that Ginsenoside Rh3 metabolized from ginsenoside Rg5 may improve chronic dermatitis or psoriasis by the regulation of IL-1beta and TNF-alpha produced by macrophage cells and of IFN-gamma produced by Th cells.

Protocol of Ginsenoside Rh3

Cell Research

Anti-inflammatory Mechanism of Ginseng Saponin Metabolite Rh3 in Lipopolysaccharide-Stimulated Microglia: Critical Role of 5'-Adenosine Monophosphate-Activated Protein Kinase Signaling Pathway.[Pubmed: 25798758]

J Agric Food Chem. 2015 Apr 8;63(13):3472-80.

Ginsenoside Rh3 is a bacterial metabolite of Rg5, which is the main constituent of heat-processed ginseng. The present study was undertaken to examine the anti-inflammatory effect of Ginsenoside Rh3 in lipopolysaccharide (LPS)-stimulated microglia.
METHODS AND RESULTS:
Ginsenoside Rh3 inhibits the expressions of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, at mRNA and protein levels, while Ginsenoside Rh3 enhanced anti-inflammatory hemeoxygenase-1 expression. Moreover, Ginsenoside Rh3 inhibited nuclear factor-κB (NF-κB) by upregulation of sirtuin 1 (SIRT1) and enhanced Nrf2 DNA-binding activities. Analysis of signaling pathways revealed that Ginsenoside Rh3 enhanced the phosphorylation of 5'-adenosine monophosphate-activated protein kinase (AMPK) and inhibited Akt and janus kinase 1 (JAK1)/signal transducer and activator of transcription 1 (STAT1) induced by LPS. By treatment of BV2 cells with AICAR (a pharmacological activator of AMPK), we found that AMPK is an upstream regulator of phosphatidylinositol 3-kinase (PI3K)/Akt and JAK1/STAT1. Furthermore, AMPK knockdown experiments demonstrated the anti-inflammatory role of AMPK in LPS/Ginsenoside Rh3 -treated BV2 microglia.
CONCLUSIONS:
Our data collectively suggest that Ginsenoside Rh3 exerts an anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways.

Animal Research

Ginsenosides Rg5 and Rh3 protect scopolamine-induced memory deficits in mice.[Pubmed: 23313392]

J Ethnopharmacol. 2013 Mar 7;146(1):294-9.

Panax ginseng (family Araliaceae) is traditionally used as a remedy for cancer, inflammation, stress and aging. To explore whether Ginsenoside Rg5 and Ginsenoside Rh3, the main constituents of heat-processed ginseng (the root of Panax ginseng), could protect memory deficit.
METHODS AND RESULTS:
We isolated Ginsenoside Rh3 and Ginsenoside Rg5 from heated-processed ginseng treated with and without human feces, respectively. Then we investigated their protective effects on memory impairment using the passive avoidance, Y-maze and Morris water maze tasks in mice. Memory deficit was induced in mice by the intraperitoneal injection of scopolamine. Ginsenoside Rg5 or Ginsenoside Rh3 increased the latency time reduced by scopolamine in passive avoidance test. Treatment with Ginsenoside Rg5 or Ginsenoside Rh3 significantly reversed the lowered spontaneous alteration induced by scopolamine in Y-maze task. Ginsenoisde Rg5 or Ginsenoside Rh3 (10 mg/kg) significantly shortened the escape latencies prolonged by treatment with scopolamine on the last day of training trial sessions in Morris water maze task. Furthermore, Ginsenoside Rg5 and GinsenosideRh3 inhibited acetylcholinesterase activity in a dose-dependent manner, with IC50 values of 18.4 and 10.2 μM, respectively. The inhibitory potency of Ginsenoside Rh3 is comparable with that of donepezil (IC50=9.9 μM). These ginsenosides also reversed hippocampal brain-derived neurotrophic factor (BDNF) expression and cAMP response element-binding protein (CREB) phosphorylation reduced by scopolamine. Of them, Ginsenoside Rh3 more potently protected memory deficit.
CONCLUSIONS:
Ginsenoside Rg5 and its metabolite Ginsenoside Rh3 may protect memory deficit by inhibiting AChE activity and increasing BDNF expression and CREB activation.

Ginsenoside Rh3 Dilution Calculator

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Ginsenoside Rh3 Molarity Calculator

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Preparing Stock Solutions of Ginsenoside Rh3

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.6533 mL 8.2664 mL 16.5328 mL 33.0655 mL 41.3319 mL
5 mM 0.3307 mL 1.6533 mL 3.3066 mL 6.6131 mL 8.2664 mL
10 mM 0.1653 mL 0.8266 mL 1.6533 mL 3.3066 mL 4.1332 mL
50 mM 0.0331 mL 0.1653 mL 0.3307 mL 0.6613 mL 0.8266 mL
100 mM 0.0165 mL 0.0827 mL 0.1653 mL 0.3307 mL 0.4133 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Ginsenoside Rh3

Ginsenoside Rh3 is a bacterial metabolite of Ginsenoside Rg5. Ginsenoside Rh3 treatment in human retinal cells induces Nrf2 activation.

In Vitro:Ginsenoside Rh3 inhibits UV-induced oxidative damages in retinal cells via activating nuclear-factor-E2-related factor 2 (Nrf2) signaling. Ginsenoside Rh3 treatment in retinal cells induces Nrf2 activation. The potential activity of Ginsenoside Rh3 is tested on Nrf2 signaling in the retinal pigment epithelium cells (RPEs). The qRT-PCR assay results demonstrate that treatment with Ginsenoside Rh3 dose-dependently increases mRNA transcription and expression of key Nrf2-regulated genes, including HO1, NQO1 and GCLC. Consequently, protein expressions of these Nrf2-dependent genes (HO1, NQO1 and GCLC) are also significantly increased in Ginsenoside Rh3 (3-10 μM)-treated RPEs. Notably, although Nrf2 mRNA level is unchanged after Ginsenoside Rh3 treatment, its protein level is significantly increased by Rh3[1]. EZ-Cytox assay is used to assess the effect of ginsenoside-Rh3 on SP 1-keratinocytes viability. Ginsenoside Rh3 (0.01, 0.1, 1 and 10 μM) shows no cytotoxic effect at all concentrations[2].

In Vivo:The potential effect of Ginsenoside Rh3 is examined on mouse retina, using the light-induced retinal damage model. Ginsenoside Rh3 intravitreal injection (5 mg/kg body weight, 30 min pre-treatment) significantly attenuates light-induced decrease of both a- and b-wave amplitude. The electroretinography (ERG)'s a-wave decreases to 46.03±1.62% % of control level after light exposure, which is back to 71.84±7.51% with Ginsenoside Rh3 administration. The b-wave is 40.19±3.34% of control level by light exposure, and Rh3 intravitreal injection brings back to 80.01±2.37% of control level[1].

References:
[1]. Tang CZ, et al. Activation of Nrf2 by Ginsenoside Rh3 protects retinal pigment epithelium cells and retinal ganglion cells from UV. Free Radic Biol Med. 2018 Mar;117:238-246. [2]. Chung I, et al. Inhibitory mechanism of Korean Red Ginseng on GM-CSF expression in UVB-irradiated keratinocytes. J Ginseng Res. 2015 Oct;39(4):322-30.

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References on Ginsenoside Rh3

Ginsenoside Rh2 and Rh3 induce differentiation of HL-60 cells into granulocytes: modulation of protein kinase C isoforms during differentiation by ginsenoside Rh2.[Pubmed:9611775]

Int J Biochem Cell Biol. 1998 Mar;30(3):327-38.

Ginsenoside Rh1 or Rh2 differentiated B16 melanoma or F9 teratocarnoma to phenotypic normal melanocyte-like cells or parietal endoderm-like cells. Ginsenoside Rh3 and Rh4 were recently isolated from Panax ginseng, but their biochemical and pharmacological effects remain unidentified. The present study investigated whether the ginsenoside Rh group (G-Rh1, -Rh2, -Rh3 and -Rh4) having similar structures induce differentiation of HL-60 cells and whether protein kinase C (PKC) is involved in differentiation by ginsenoside. Differentiation was assessed by Wright-Giemsa stain and nitroblue tetrazolium reduction. G-Rh2 and G-Rh3 induced differentiation of HL-60 cells into morphologically and functionally granulocytes but G-Rh1 and G-Rh4 did not. G-Rh2 and G-Rh3 arrested the cell cycle at the G1/S phase, consistent with the ability to induce differentiation in a decreasing order of retinoic acid > G-Rh2 > G-Rh3. During differentiation by G-Rh2, Ca2+/phospholipid-dependent PKC activity was increased in both the cytosol and total cell extract and Ca2+/phospholipid-dependent phosphorylation of 38 and 200 kDa endogenous proteins increased, while phosphorylation of 60, 64, 66 and 97 kDa proteins was Ca2+/phospholipid-independent. When cytosolic PKC isoforms were analyzed by immunoblotting, no significant change was observed in the alpha level, however, the immunoreactive 60 kDa band of a similar mass to the PKC catalytic fragment appeared following treatment with G-Rh2. The beta isoform was gradually increased with prolonged treatment. The gamma isoform was not detected in the cytosol of untreated cells, whereas a small amount was detected 5 days after treatment. It is concluded that G-Rh2 and G-Rh3 can induce differentiation of HL-60 cells into granulocytes and modulation of PKC isoform levels may contribute to differentiation of HL-60 cells by G-Rh2.

Anti-inflammatory mechanism of ginseng saponin metabolite Rh3 in lipopolysaccharide-stimulated microglia: critical role of 5'-adenosine monophosphate-activated protein kinase signaling pathway.[Pubmed:25798758]

J Agric Food Chem. 2015 Apr 8;63(13):3472-80.

Ginsenoside Rh3 is a bacterial metabolite of Rg5, which is the main constituent of heat-processed ginseng. The present study was undertaken to examine the anti-inflammatory effect of Ginsenoside Rh3 in lipopolysaccharide (LPS)-stimulated microglia. Rh3 inhibits the expressions of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-6, at mRNA and protein levels, while Rh3 enhanced anti-inflammatory hemeoxygenase-1 expression. Moreover, Rh3 inhibited nuclear factor-kappaB (NF-kappaB) by upregulation of sirtuin 1 (SIRT1) and enhanced Nrf2 DNA-binding activities. Analysis of signaling pathways revealed that Rh3 enhanced the phosphorylation of 5'-adenosine monophosphate-activated protein kinase (AMPK) and inhibited Akt and janus kinase 1 (JAK1)/signal transducer and activator of transcription 1 (STAT1) induced by LPS. By treatment of BV2 cells with AICAR (a pharmacological activator of AMPK), we found that AMPK is an upstream regulator of phosphatidylinositol 3-kinase (PI3K)/Akt and JAK1/STAT1. Furthermore, AMPK knockdown experiments demonstrated the anti-inflammatory role of AMPK in LPS/Rh3-treated BV2 microglia. Our data collectively suggest that Rh3 exerts an anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways.

Ginsenosides Rg5 and Rh3 protect scopolamine-induced memory deficits in mice.[Pubmed:23313392]

J Ethnopharmacol. 2013 Mar 7;146(1):294-9.

ETHNOPHARMACOLOGICAL RELEVANCE: Panax ginseng (family Araliaceae) is traditionally used as a remedy for cancer, inflammation, stress and aging. AIM OF STUDY: To explore whether ginsenosides Rg5 and Rh3, the main constituents of heat-processed ginseng (the root of Panax ginseng), could protect memory deficit. MATERIALS AND METHODS: We isolated ginsenosides Rh3 and Rg5 from heated-processed ginseng treated with and without human feces, respectively. Then we investigated their protective effects on memory impairment using the passive avoidance, Y-maze and Morris water maze tasks in mice. Memory deficit was induced in mice by the intraperitoneal injection of scopolamine. RESULTS: Ginsenosides Rg5 or Rh3 increased the latency time reduced by scopolamine in passive avoidance test. Treatment with ginsenoside Rg5 or Rh3 significantly reversed the lowered spontaneous alteration induced by scopolamine in Y-maze task. Ginsenoisde Rg5 or Rh3 (10 mg/kg) significantly shortened the escape latencies prolonged by treatment with scopolamine on the last day of training trial sessions in Morris water maze task. Furthermore, ginsenosides Rg5 and Rh3 inhibited acetylcholinesterase activity in a dose-dependent manner, with IC50 values of 18.4 and 10.2 muM, respectively. The inhibitory potency of Ginsenoside Rh3 is comparable with that of donepezil (IC50=9.9 muM). These ginsenosides also reversed hippocampal brain-derived neurotrophic factor (BDNF) expression and cAMP response element-binding protein (CREB) phosphorylation reduced by scopolamine. Of them, Ginsenoside Rh3 more potently protected memory deficit. CONCLUSIONS: Ginsenoside Rg5 and its metabolite Ginsenoside Rh3 may protect memory deficit by inhibiting AChE activity and increasing BDNF expression and CREB activation.

Inhibitory effect of ginsenoside Rg5 and its metabolite ginsenoside Rh3 in an oxazolone-induced mouse chronic dermatitis model.[Pubmed:16964764]

Arch Pharm Res. 2006 Aug;29(8):685-90.

The effect of a main constituent ginsenoside Rg5 isolated from red ginseng and its metabolite Ginsenoside Rh3 in a chronic dermatitis model was investigated. Ginsenosides Rg5 and Rh3 suppressed swelling of oxazolone-induced mouse ear contact dermatitis. These ginsenosides also reduced mRNA expressions of cyclooxygenase-2, interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma. The inhibition of Ginsenoside Rh3 was more potent than that of ginsenoside Rg5. These findings suggest that Ginsenoside Rh3 metabolized from ginsenoside Rg5 may improve chronic dermatitis or psoriasis by the regulation of IL-1beta and TNF-alpha produced by macrophage cells and of IFN-gamma produced by Th cells.

Description

Ginsenoside Rh3 is a bacterial metabolite of Ginsenoside Rg5. Ginsenoside Rh3 treatment in human retinal cells induces Nrf2 activation.

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