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    Ginsenoside Rc
    CAS No. 11021-14-0 Price $100 / 20mg
    Catalog No.CFN99973Purity>=98%
    Molecular Weight1079.27Type of CompoundTriterpenoids
    FormulaC53H90O22Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Ginsenoside Rc exhibits anti-diabetic, anti-adipogenic, anticancer and anti-inflammatory activities; it can attenuate inflammatory symptoms of gastritis, hepatitis and arthritis, and it can significantly enhance glucose uptake by inducing ROS generation, which leads to AMPK and p38 MAPK activation. Rc enhances GABA receptorA (GABAA)-mediated ion channel currents (IGABA), it also inhibits the expression of TNF-α and IL-1β.
    Targets: PPAR | AP-1 | PI3K | Akt | AMPK | PKB | p38MAPK | ROS | IL Receptor | cAMP | TNF-α | NF-kB | GABA receptor
    In vitro:
    Molecules. 2015 Jan 14;20(1):1293-303.
    Ginsenoside Rc promotes anti-adipogenic activity on 3T3-L1 adipocytes by down-regulating C/EBPα and PPARγ.[Pubmed: 25594343]
    Panax ginseng and its major components, the ginsenosides, are widely used in oriental medicine for the prevention of various disorders.
    In the present study, the inhibitory activity of Ginsenoside Rc on adipogenesis was investigated using the 3T3-L1 cell line. The results obtained showed that Rc reduced the proliferation and viability of 3T3-L1 preadipocytes in a dose-dependent manner. Treatment with Rc decreased the number of adipocytes and reduced lipid accumulation in maturing 3T3-L1 preadipocytes, demonstrating an inhibitory effect on lipogenesis. Moreover, it was found that Rc directly induced lipolysis in adipocytes and down-regulated the expression of major transcription factors of the adipogenesis pathway, such as PPARγ and C/EBPα.
    These findings indicate that Rc is capable of suppressing adipogenesis and therefore they seem to be natural bioactive factors effective in adipose tissue mass modulation.
    Arch Pharm Res. 2003 Jan;26(1):53-7.
    Ginsenoside Rc and Re stimulate c-fos expression in MCF-7 human breast carcinoma cells.[Pubmed: 12568359]
    We have found that Ginsenoside Rc and Re induce c-fos in MCF-7 human breast carcinoma cells at both the mRNA and protein levels. However, neither ginsenoside activated the expression of reporter gene under the control of AP-1/TPA response elements.
    We have also examined the possibility that Ginsenoside Rc and Re act by binding to intracellular steroid hormone receptors that act as transcriptional factors in the nucleus in inducing c-fos mRNA in MCF7 human breast carcinoma cells. However, Ginsenoside Rc and Re did not bind to glucocorticoid, androgen, estrogen, or retinoic acid receptors as examined by the transcription activation of the luciferase reporter genes in CV-1 cells that were transiently transfected with the corresponding steroid hormone receptors and hormone responsive luciferase reporter plasmids.
    These data demonstrate that Ginsenoside Rc and Re act via other transcription factors and not via estrogen receptor in c-Fos expression.
    In vivo:
    Am J Chin Med. 2016;44(3):595-615.
    Ginsenoside Rc from Korean Red Ginseng (Panax ginseng C.A. Meyer) Attenuates Inflammatory Symptoms of Gastritis, Hepatitis and Arthritis.[Pubmed: 27109153 ]
    Korean Red Ginseng (KRG) is an herbal medicine prescribed worldwide that is prepared from Panax ginseng C.A. Meyer (Araliaceae). Out of ginseng's various components, ginsenosides are regarded as the major ingredients, exhibiting anticancer and anti-inflammatory activities. Although recent studies have focused on understanding the anti-inflammatory activities of KRG, compounds that are major anti-inflammatory components, precisely how these can suppress various inflammatory processes has not been fully elucidated yet. In this study, we aimed to identify inhibitory saponins, to evaluate the in vivo efficacy of the saponins, and to understand the inhibitory mechanisms.
    To do this, we employed in vitro lipopolysaccharide-treated macrophages and in vivo inflammatory mouse conditions, such as collagen (type II)-induced arthritis (CIA), EtOH/HCl-induced gastritis, and lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-triggered hepatitis. Molecular mechanisms were also verified by real-time PCR, immunoblotting analysis, and reporter gene assays. Out of all the ginsenosides, Ginsenoside Rc (G-Rc) showed the highest inhibitory activity against the expression of tumor necrosis factor (TNF)-[Formula: see text], interleukin (IL)-1[Formula: see text], and interferons (IFNs). Similarly, this compound attenuated inflammatory symptoms in CIA, EtOH/HCl-mediated gastritis, and LPS/D-galactosamine (D-GalN)-triggered hepatitis without altering toxicological parameters, and without inducing gastric irritation. These anti-inflammatory effects were accompanied by the suppression of TNF-[Formula: see text] and IL-6 production and the induction of anti-inflammatory cytokine IL-10 in mice with CIA. G-Rc also attenuated the increased levels of luciferase activity by IRF-3 and AP-1 but not NF-[Formula: see text]B. In support of this phenomenon, G-Rc reduced TBK1, IRF-3, and ATF2 phosphorylation in the joint and liver tissues of mice with hepatitis.
    Therefore, our results strongly suggest that G-Rc may be a major component of KRG with useful anti-inflammatory properties due to its suppression of IRF-3 and AP-1 pathways.
    Ginsenoside Rc Description
    Source: The roots of Panax ginseng C. A. Mey.
    Solvent: DMSO, 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.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 0.9266 mL 4.6328 mL 9.2655 mL 18.531 mL 23.1638 mL
    5 mM 0.1853 mL 0.9266 mL 1.8531 mL 3.7062 mL 4.6328 mL
    10 mM 0.0927 mL 0.4633 mL 0.9266 mL 1.8531 mL 2.3164 mL
    50 mM 0.0185 mL 0.0927 mL 0.1853 mL 0.3706 mL 0.4633 mL
    100 mM 0.0093 mL 0.0463 mL 0.0927 mL 0.1853 mL 0.2316 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.
    Kinase Assay:
    J Ethnopharmacol. 2010 Feb 17;127(3):771-6.
    Ginsenoside Rc, an active component of Panax ginseng, stimulates glucose uptake in C2C12 myotubes through an AMPK-dependent mechanism.[Pubmed: 19961916 ]
    Panax ginseng and its major component, ginsenosides, are widely used for the prevention of various disorders in oriental medicine. To evaluate the effect of Ginsenoside Rc (Rc), one of the active constituents in Panax ginseng, on glucose uptake in C2C12 myotubes.
    Treatment of the C2C12 myotubes with Rc significantly increased glucose uptake. To determine the mechanism of Rc-induced glucose uptake, either insulin-dependent signaling or insulin-independent signaling pathway activities were measured using western blot analysis. We showed that Rc significantly activated an insulin-independent AMPK signaling pathway. However, Rc had no effect on the components of the insulin-dependent signaling pathway, such as receptor substrates (IRS)-1 and protein kinase B or Akt (PKB/Akt). Moreover, we found that treatment with an AMPK inhibitor abolished both glucose uptake and p38 MAPK phosphorylation. This result implies that AMPK activity is critical for the Rc-induced glucose uptake and that AMPK is situated upstream of p38 MAPK. In addition, we also showed that the activation of AMPK and p38 induced by Ginsenoside Rc is mediated by reactive oxygen species (ROS) production, suggesting that upstream regulators of AMPK- and p38 MAPK-mediated glucose uptake.
    Ginsenoside Rc significantly enhances glucose uptake by inducing ROS generation, which leads to AMPK and p38 MAPK activation. Consequently, Ginsenoside Rc can be used as a potent natural anti-diabetic agent.
    Cell Research:
    Arch Pharm Res. 2014 Jun;37(6):813-20.
    Ginsenoside Rc modulates Akt/FoxO1 pathways and suppresses oxidative stress.[Pubmed: 23918648]
    Ginsenoside Rc (Rc), a protopanaxadiol type ginsenoside, is the active component mainly responsible for the therapeutic and pharmacologic properties of ginseng, which are derived from its suppression of superoxide-induced free radicals. Forkhead box O (FoxO1) regulates various genes involved in cellular metabolism related to cell death and response to oxidative stress, and Rc is known to prevent FoxO1 phosphorylation by activation of PI3K/Akt and subsequent inhibition of AMP-activated protein kinase (AMPK) in cells exposed to tert-butylhydroperoxide (t-BHP).
    In the current study, we attempted the mechanism of increased catalase expression by Rc through inhibition of FoxO1 activation resulting from t-BHP-induced production of reactive species (RS). We found that overexpression of catalase induced by Rc resulted in suppression of RS production in kidney human embryo kidney 293T cells (HEK293T) cells, and that oxidative stress induced activation of PI3K/Akt and inhibition of the AMPK pathway and FoxO1 phosphorylation, leading to down-regulation of catalase, a FoxO1-targeting gene. In addition, treatment of HEK293T cells with Rc resulted in cAMP-response element-binding protein (CREB)-binding protein (CBP) regulated FoxO1 acetylation.
    Our results suggest that Rc modulates FoxO1 phosphorylation through activation of PI3K/Akt and inhibition of AMPK and FoxO1 acetylation through interaction with CBP and SIRT1, and that this leads to upregulation of catalase under conditions of oxidative stress.