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    Ginsenoside Rh3
    CAS No. 105558-26-7 Price $218 / 20mg
    Catalog No.CFN99972Purity>=98%
    Molecular Weight604.86Type of CompoundTriterpenoids
    FormulaC36H60O7Physical DescriptionWhite powder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Ginsenoside Rh3 Description
    Source: The roots of Panax ginseng C. A. Mey.
    Biological Activity or Inhibitors: 1. Ginsenoside Rh3 is a bacterial metabolite of Rg5, has anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways.
    2. Ginsenosides Rh3 and Rg5 can suppress swelling of oxazolone-induced mouse ear contact dermatitis, ginsenoside Rh3 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.
    3. Ginsenoside-Rh2 and 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.
    4. Ginsenosides Rg5 and Rh3 inhibit 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.
    Solvent: Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
    Calculate Dilution Ratios(Only for Reference)
    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 need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Ginsenoside Rh3 References Information
    Citation [1]

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

    Inhibitory effect of ginsenoside Rg5 and its metabolite ginsenoside Rh3 in an oxazolone-induced mouse chronic dermatitis model.[Pubmed: 16964764]
    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.
    Citation [2]

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

    Ginsenosides Rg5 and Rh3 protect scopolamine-induced memory deficits in mice.[Pubmed: 23313392]
    To explore whether ginsenoside Rg5 and Ginsenoside Rh3, the main constituents of heat-processed ginseng (the root of Panax ginseng), could protect memory deficit. 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, ginsenosides Rg5 and Ginsenoside Rh3 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.
    Citation [3]

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

    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]
    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 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. 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.
    Citation [4]

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

    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]
    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.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. Our data collectively suggest that Ginsenoside Rh3 exerts an anti-inflammatory effect in microglia by modulating AMPK and its downstream signaling pathways.