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    Ginsenoside Re
    CAS No. 52286-59-6 Price $50 / 20mg
    Catalog No.CFN99974Purity>=98%
    Molecular Weight947.15Type of CompoundTriterpenoids
    FormulaC48H82O18Physical DescriptionWhite powder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Ginsenoside Re Description
    Source: The roots of Panax ginseng C. A. Mey.
    Biological Activity or Inhibitors: 1. Ginsenoside Re is an effective antidiabetic agent via significant antioxidant efficacy, particularly in the prevention of diabetic microvasculopathy.
    2. Ginsenoside Re is a protective agent for the heart against ischemia, by enhancing the slowly activating component of the delayed rectifier K+ current (IKs) and suppresses the L-type Ca2+ current (ICa,L) to shorten action potential duration(APD).
    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 1.0558 mL 5.279 mL 10.558 mL 21.116 mL 26.395 mL
    5 mM 0.2112 mL 1.0558 mL 2.1116 mL 4.2232 mL 5.279 mL
    10 mM 0.1056 mL 0.5279 mL 1.0558 mL 2.1116 mL 2.6395 mL
    50 mM 0.0211 mL 0.1056 mL 0.2112 mL 0.4223 mL 0.5279 mL
    100 mM 0.0106 mL 0.0528 mL 0.1056 mL 0.2112 mL 0.2639 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 Re References Information
    Citation [1]

    Cell Mol Neurobiol. 2015 Mar 17.

    Ginsenoside Re Promotes Nerve Regeneration by Facilitating the Proliferation, Differentiation and Migration of Schwann Cells via the ERK- and JNK-Dependent Pathway in Rat Model of Sciatic Nerve Crush Injury.[Pubmed: 25776135]
    Exploring effective drugs that are capable of promoting nerve regeneration has gained much attention. Ginsenoside Re (Re) is the main ingredient of ginseng berries and roots. Research in the area has shown that Ginsenoside Re exhibits multiple pharmacological activities via different mechanisms both in vivo and in vitro. But the potential therapeutic effects of Ginsenoside Re on sciatic nerve crush injury (SNC) have been little investigated. Herein, we investigated the protect effect of Ginsenoside Re on peripheral nerve regeneration in a rat SNC model. Walking track analysis revealed that Ginsenoside Re treatment significantly promoted functional recovery of crushed sciatic nerve in rats. The expression of PCNA in rat sciatic nerve was up-regulated by Ginsenoside Re treatment, and peaked when the concentration of Ginsenoside Re was 2.0 mg/kg. Using immunofluorescent staining, we found that Ginsenoside Re greatly increased the expression of GAP-43 and S100 in injured rat sciatic nerve. Furthermore, we evaluated the effects of Ginsenoside Re on proliferation, differentiation, and migration of Schwann cells in SNC rat models. Our studies reveal that Ginsenoside Re promotes nerve regeneration is depend on ERK1/2 and JNK1/2 signaling pathway. Elevated Oct-6 expression and featured morphological changes indicated that Ginsenoside Re facilitated the differentiation of Schwann cells following SNC. Also, transwell and wound-healing assay demonstrated that the migration capabilities of Schwann cell were significantly enhanced after Ginsenoside Re treatment.
    Citation [2]

    J Appl Toxicol. 2014 Dec 18.

    Ginsenoside Re protects methamphetamine-induced mitochondrial burdens and proapoptosis via genetic inhibition of protein kinase C δ in human neuroblastoma dopaminergic SH-SY5Y cell lines.[Pubmed: 25523949]
    Recently, we have demonstrated that Ginsenoside Re protects methamphetamine (MA)-induced dopaminergic toxicity in mice via genetic inhibition of PKCδ and attenuation of mitochondrial stress. In addition, we have reported that induction of mitochondrial glutathione peroxidase (GPx) is also important for neuroprotection mediated by Ginsenoside Re. To extend our knowledge, we examined the effects of Ginsenoside Re against MA toxicity in vitro condition using SH-SY5Y neuroblastoma cells. Treatment with Ginsenoside Re resulted in significant attenuations against a decrease in the activity of GPx and an increase in the activity of superoxide dismutase (SOD) in the cytosolic and mitochondrial fraction. The changes in glutathione (GSH) paralleled those in GPx in the same experimental condition. Consistently, Ginsenoside Re treatment exhibited significant protections against cytosolic and mitochondrial oxidative damage (i.e. lipid peroxidation and protein oxidation), mitochondrial translocation of PKCδ, mitochondrial dysfunction (mitochondrial transmembrane potential and intra-mitochondrial Ca2+ ), apoptotic events [i.e., cytochrome c release from mitochondria, cleavage of caspase-3 and poly(ADP-ribose)polymerase-1, nuclear condensation, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive apoptotic cells], and a reduction in the tyrosine hydroxylase (TH) expression and TH activity induced by MA in SH-SY5Y neuroblastoma cells. These protective effects of Ginsenoside Re were comparable to those of PKCδ antisense oligonucleotide (ASO). However, Ginsenoside Re did not significantly provide additional protective effects mediated by genetic inhibition of PKCδ. Our results suggest that PKCδ is a specific target for Ginsenoside Re-mediated protective activity against MA toxicity in SH-SY5Y neuroblastoma cells.
    Citation [3]

    Life Sci. 2014 Oct 12;115(1-2):15-21.

    Ginsenoside Re enhances small-conductance Ca(2+)-activated K(+) current in human coronary artery endothelial cells.[Pubmed: 25242515 ]
    The objectives of this study, therefore, were to test 1) whether vasorelaxing Ginsenoside Re could affect KCa current, an important regulator of NO production, in human coronary artery endothelial cells (HCAECs); and 2) whether small-conductance KCa (SKCa) channel was the channel subtype involved. Ionic currents of cultured HCAECs were studied using whole-cell patch clamp technique. Ginsenoside Re dose-dependently increased endothelial outward currents, with an EC50 of 408.90±1.59nM, and a maximum increase of 36.20±5.62% (mean±SEM; p<0.05). Apamin, an SKCa channel inhibitor, could block this effect, while La(3+), a nonselective cation channel (NSC) blocker, could not. When NSC channel, inward-rectifier K(+) channel, intermediate-, and large-conductance KCa channels were simultaneously blocked, Ginsenoside Re could still increase outward currents significantly (35.49±4.22%; p<0.05); this effect was again abolished by apamin. Repeating the experiments when Cl(-) channel was additionally blocked gave similar results. Finally, we demonstrated that Ginsenoside Re could hyperpolarize HCAECs; this effect was reversed by apamin. These data clearly indicate that Ginsenoside Re increased HCAEC outward current via SKCa channel activation, and NSC channel was not involved. This is the first report to demonstrate that Ginsenoside Re could increase SKCa channel activity in HCAECs. This can be a mechanism mediating ginseng's beneficial actions on coronary vessels.
    Citation [4]

    Planta Med. 2014 Aug;80(13):1143-50.

    Establishment of an enzyme-linked immunosorbent assay and application on determination of ginsenoside Re in human saliva.[Pubmed: 25197955]
    This work describes an immunochemical approach for the quality control of Panax ginseng and a pharmacological study of Ginsenoside Re, a major bioactive constituent in P. ginseng, using an enzyme-linked immunosorbent assay. A hybridoma secreting monoclonal antibody against Ginsenoside Re was produced by fusing splenocytes immunized with a Ginsenoside Re-bovine serum albumin conjugate with the hypoxanthine-aminopterin-thymidine-sensitive mouse myeloma SP2/0 cell line. The method, at an effective measuring range of 7.8-500 ng · mL(-1) of Ginsenoside Re, successfully detected Ginsenoside Re in Chinese traditional herb prescriptions. The results demonstrate that we generated a novel and reliable assay system for measuring Ginsenoside Re in Chinese medicines more efficiently. Futhermore, we determined the Ginsenoside Re concentrations in the saliva of six healthy adults after the oral administration of a ginseng capsule to study the pharmacokinetics of Ginsenoside Re in human saliva.