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    Ginsenoside Rg2
    Information
    CAS No. 52286-74-5 Price $80 / 20mg
    Catalog No.CFN99968Purity>=98%
    Molecular Weight785.02Type of CompoundTriterpenoids
    FormulaC42H72O13Physical DescriptionWhite powder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Ginsenoside Rg2 Description
    Source: The roots of Panax ginseng C. A. Mey.
    Biological Activity or Inhibitors: 1. Ginsenoside Rg2 suppresses the hepatic glucose production via AMPK-induced phosphorylation of GSK3β and induction of SHP gene expression, suggests that it has therapeutic potential for type 2 diabetic patients.
    2. Ginsenoside Rg2 inhibits nicotinic acetylcholine receptor-mediated Na+ influx and channel activity; it also inhibits the 5-HT-induced inward peak current (I5-HT) in dose dependent and reversible manner, the half-inhibitory concentrations (IC50) of ginsenoside Rg2 is 22.3 +/- 4.6 microM, suggests that it might regulate the 5-HT3A receptors that are expressed in Xenopus oocytes.
    3. Ginsenoside Rg2 can reduce LPS-mediated THP-1 monocyte adhesion to HUVEC, in a concentration-dependent manner, it may provide direct vascular benefits with inhibition of leukocyte adhesion into vascular wall thereby providing protection against vascular inflammatory disease.
    4. Ginsenoside Rg2 protects cells against UVB-induced genotoxicity by increasing DNA repair, in possible association with modulation of protein levels involved in p53 signaling pathway.
    5. Ginsenoside Rg2 improves learning and memory through mechanisms related to anti-apoptosis in MID rats, indicates that it may represent a potential neurorestorative treatment strategy for vascular dementia or other ischemic insults.
    6. Ginsenoside Rg2 has protective effects against H2O2-induced injury and apoptosis in H9c2 cells.
    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.
    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
    doi: 10.1016/j.cell.2017.12.019.

    PMID: 29328914

    Mol Cell. 2017 Nov 16;68(4):673-685.e6.
    doi: 10.1016/j.molcel.2017.10.022.

    PMID: 29149595

    Scientific Reports 2017 Dec 11;7(1):17332.
    doi: 10.1038/s41598-017-17427-6.

    PMID: 29230013

    Molecules. 2017 Oct 27;22(11). pii: E1829.
    doi: 10.3390/molecules22111829.

    PMID: 29077044

    J Cell Biochem. 2018 Feb;119(2):2231-2239.
    doi: 10.1002/jcb.26385.

    PMID: 28857247

    Phytomedicine. 2018 Feb 1;40:37-47.
    doi:10.1016/j.phymed.2017.12.030

    PMID: 29496173
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.2739 mL 6.3693 mL 12.7385 mL 25.4771 mL 31.8463 mL
    5 mM 0.2548 mL 1.2739 mL 2.5477 mL 5.0954 mL 6.3693 mL
    10 mM 0.1274 mL 0.6369 mL 1.2739 mL 2.5477 mL 3.1846 mL
    50 mM 0.0255 mL 0.1274 mL 0.2548 mL 0.5095 mL 0.6369 mL
    100 mM 0.0127 mL 0.0637 mL 0.1274 mL 0.2548 mL 0.3185 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 Rg2 References Information
    Citation [1]

    Korean J Physiol Pharmacol. 2013 Apr;17(2):133-7.

    Ginsenoside rg2 inhibits lipopolysaccharide-induced adhesion molecule expression in human umbilical vein endothelial cell.[Pubmed: 23626475]
    Vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), P- and E-selectin play a pivotal role for initiation of atherosclerosis. Ginsenoside, a class of steroid glycosides, is abundant in Panax ginseng root, which has been used for prevention of illness in Korea. In this study, we investigated the mechanism(s) by which Ginsenoside Rg2 may inhibit VCAM-1 and ICAM-1 expressions stimulated with lipopolysaccharide (LPS) in human umbilical vein endothelial cell (HUVEC). LPS increased VCAM-1 and ICAM-1 expression. Ginsenoside Rg2 prevented LPS-mediated increase of VCAM-1 and ICAM-1 expression. On the other hand, JSH, a nuclear factor kappa B (NF-κB) inhibitor, reduced both VCAM-1 and ICAM-1 expression stimulated with LPS. SB202190, inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), and wortmannin, phosphatidylinositol 3-kinase (PI3-kinase) inhibitor, reduced LPS-mediated VCAM-1 but not ICAM-1 expression. PD98059, inhibitor of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) did not affect VCAM-1 and ICAM-1 expression stimulated with LPS. SP600125, inhibitor of c-Jun N-terminal kinase (JNK), reduced LPS-mediated ICAM-1 but not VCAM-1 expression. LPS reduced IkappaBα (IκBα) expression, in a time-dependent manner within 1 hr. Ginsenoside Rg2 prevented the decrease of IκBα expression stimulated with LPS. Moreover, Ginsenoside Rg2 reduced LPS-mediated THP-1 monocyte adhesion to HUVEC, in a concentration-dependent manner. These data provide a novel mechanism where the Ginsenoside Rg2 may provide direct vascular benefits with inhibition of leukocyte adhesion into vascular wall thereby providing protection against vascular inflammatory disease.
    Citation [2]

    Chem Biol Interact. 2012 Jan 5;195(1):35-42.

    Ginsenoside Rg2 induces orphan nuclear receptor SHP gene expression and inactivates GSK3β via AMP-activated protein kinase to inhibit hepatic glucose production in HepG2 cells.[Pubmed: 22062806]
    Panax ginseng is known to have anti-diabetic activity, but the active ingredients have not been fully explored yet. Here, we test whether Ginsenoside Rg2 has an inhibitory effect on hepatic glucose production and determine its mechanism of action. Ginsenoside Rg2 significantly inhibits hepatic glucose production and induces phosphorylations of liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK) and glycogen synthase kinase 3β (GSK3β) in time- and concentration-dependent manners in human HepG2 hepatoma cells, and these effects were abolished in the presence of compound C, a selective AMPK inhibitor. In addition, phosphorylated form of cAMP-response element-binding protein (CREB), a key transcription factor for hepatic gluconeogenesis, was decreased in time- and concentration-dependent manners. Next, gene expression of orphan nuclear receptor small heterodimer partner (SHP) was also examined. Ginsenoside Rg2 markedly enhanced the gene expression of SHP and its direct interaction with CREB, which results in disruption of CREB·CRTC2 complex. Consequently, expressions of relevant genes such as peroxisome proliferation-activated receptor γ coactivator-1α (PGC-1α), phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) were all significantly suppressed and these effects were also reversed in the presence of compound C. In conclusion, our results propose that Ginsenoside Rg2 suppresses the hepatic glucose production via AMPK-induced phosphorylation of GSK3β and induction of SHP gene expression. Further studies are warranted to elucidate a therapeutic potential of Ginsenoside Rg2 for type 2 diabetic patients.
    Citation [3]

    Int J Clin Exp Med. 2015 Nov 15;8(11):19938-47.

    Protective effects of ginsenoside Rg2 against H2O2-induced injury and apoptosis in H9c2 cells.[Pubmed: 26884906]
    Ginsenoside Rg2 is one of the major active components of ginseng and has many biological activities. This study aimed to investigate the protective effects of Ginsenoside Rg2 against H2O2-induced injury and apoptosis in H9c2 cells. The results showed that pretreatment with Ginsenoside Rg2 not only increased cell viability, but also decreased lactate dehydrogenase (LDH) release. Ginsenoside Rg2 inhibited the decrease of SOD, GSH-PX activities and the increase of MDA content induced by H2O2. Meanwhile, the levels of ROS generation and cardiomyocyte apoptosis in Ginsenoside Rg2 group significantly reduced when compared with the model group. Western blot analyses demonstrated that Ginsenoside Rg2 up-regulate level of Bcl-2 expression and down-regulate levels of Bax, Caspase-3, -9 expression. These findings indicated that Ginsenoside Rg2 could protect H9c2 cells against H2O2-induced injury through its actions of anti-oxidant and anti-apoptosis.
    Citation [4]

    Naunyn Schmiedebergs Arch Pharmacol. 2010 Jul;382(1):89-101.

    Effects of ginsenoside Rg2 on the ultraviolet B-induced DNA damage responses in HaCaT cells.[Pubmed: 20508917]
    RT-PCR analysis showed that the Ginsenoside Rg2(Rg2)-alone treatment slightly upregulated the p53 and GADD45 transcript and protein levels by about 1.5-fold as compared with the nontreated control. The mRNA levels of p53 and GADD45 in cells exposed to UVB and post-incubated with Rg2 for 24 h decreased in an Rg2 concentration-dependent manner as compared with that post-incubated in normal medium. However, the mRNA level of the UVB-exposed cells post-incubated with 5 microM retinol was essentially the same as that post-incubated in normal medium. Time course experiment showed that the mRNA levels of p53 and GADD45 in UVB-exposed cells were upregulated by post-incubation with 50 microM Rg2 until 6 and 9 h, respectively, and then gradually decreased until 24 h. By Western blot analysis, it was also revealed that the Rg2 post-incubation decreases the expression of p53, phospho-p53, GADD45, and ATM in UVB-exposed cells. Time course analysis also indicated that these decreased expressions were due to the earlier upregulation of p53 and GADD45 proteins. When UVB-exposed cells were post-incubated with Rg2 for 24 h after UVB exposure, the level of remaining cyclobutane pyrimidine dimers decreased in both Rg2 concentration- and time-dependent manner. All these results suggest that Rg2 protects cells against UVB-induced genotoxicity by increasing DNA repair, in possible association with modulation of protein levels involved in p53 signaling pathway.
    Citation [5]

    Progress in Modern Biomedicine, 2010,10(06):1069-75.

    Ginsenoside Rg2 attenuates learning and memory loss through an anti-apoptotic property in a rat model of multi-infarct dementia.[Reference: WebLink]
    We evaluated the neurorestorative effects of Ginsenoside Rg2,one of the main bioactive components of Panax ginseng,in a rat model of multi-infarct dementia (MID).Methods: A MID rat model was established as produced by multiple cerebral infarctions induced by means of a thrombo-inducer.Y-maze learning performance was assessed after thrombo-induction.Results: Immunocytochemical techniques were employed to assess cell apoptosis as measured by protein expressions of glutamate,calpainⅡ,caspase-3 and bax.Learning and memory performance were impaired by thrombo-inductor induced MID and the expression of glutamate,calpainⅡ,caspase-3 and bax were increased in this MID rat model.After Ginsenoside Rg2 (2.5,5 or 10 mg/kg) or nimodipine (50μg/kg) treatment,learning and memory performance was increased and the expression of glutamate,calpain Ⅱ,caspase-3 and bax were decreased in this MID model.Conclusion: These findings suggest that Ginsenoside Rg2 improved learning and memory through mechanisms related to anti-apoptosis in MID rats.These results also indicate that Ginsenoside Rg2 may represent a potential neurorestorative treatment strategy for vascular dementia or other ischemic insults.
    Citation [6]

    Mol Cells. 2003 Feb 28;15(1):34-9.

    Effects of ginsenosides on glycine receptor alpha1 channels expressed in Xenopus oocytes.[Pubmed: 12661758]
    Ginsenosides, major active ingredients of Panax ginseng, are known to regulate the excitatory ligand-gated ion channel activity. Recent reports showed that ginsenosides attenuate nicotinic acetylcholine and NMDA receptor channel activity. However, it is not known whether ginsenosides also affect the inhibitory ligand-gated ion channel activity. We investigated the effect of ginsenosides on human glycine alpha1 receptor channel activity expressed in Xenopus oocytes using a two-electrode voltage clamp technique. Treatment of ginsenoside Rf enhances glycine-induced inward peak current (IGly) with dose dependent and reversible manner but ginsenoside Rf itself did not elicit membrane currents. The half-stimulatory concentrations (EC50) of ginsenoside Rf was 49.8 +/- 8.9 microM. Glycine receptor antagonist strychnine completely blocked the inward current elicited by glycine plus ginsenoside Rf. Cl- channel blocker 4,4'-disothiocyanostilbene-2,2'-disulfonic acid (DIDS) also blocked the inward current elicited by glycine plus ginsenoside Rf. We also tested the effect of eight individual ginsenosides (i.e., Rb1, Rb2, Rc, Rd, Re, Rg1, Ginsenoside Rg2, and Ro) in addition to ginsenoside Rf. We found that five of them significantly enhanced the inward current induced by glycine with the following order of potency: Rb1 > Rb2 > Ginsenoside Rg2 > or = Rc > Rf > Rg1 > Re. These results indicate that ginsenosides might regulate gylcine receptor expressed in Xenopus oocytes and this regulation might be one of the pharmacological actions of Panax ginseng.