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    Ginsenoside Rg2
    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 has a neuroprotective effect against glutamate-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis.
    2. Ginsenoside Rg2 may be as a potential treatment strategy for Alzheimer's disease by inhibiting the formation of Abeta1-40.
    3. Ginsenoside Rg2 inhibits nicotinic acetylcholine receptor-mediated Na+ influx and channel activity.
    4. Ginsenoside Rg2 may regulate the 5-HT3A receptors that are expressed in Xenopus oocytes.
    5. Ginsenoside Rg2 may inhibit or prevent the growth of tumors.
    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 1.2739 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]

    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]
    In the present study, the effects of purified Ginsenoside Rg2 on the repair and apoptosis in ultraviolet B (UVB)-exposed HaCaT cells were investigated on gene expression levels. When cells were exposed to UVB and post-incubated in normal medium for 24 h, the cell viability decreased to about 50% of that in nontreated control. When Ginsenoside Rg2 was post-incubated, however, the UVB-induced cytotoxicity was significantly prevented in an Ginsenoside Rg2 concentration- and time-dependent manner. The apoptotic nuclear fragmentation resulting from UVB exposure was also significantly protected by the Ginsenoside Rg2 post-incubation. Microarray analysis showed that the genes stimulated by the Ginsenoside Rg2 alone treatment include those involved in p53 signaling pathway such as GADD45alpha, GADD45beta, and cell communication genes. RT-PCR analysis showed that the Ginsenoside 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 Ginsenoside Rg2 for 24 h decreased in an Ginsenoside 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 Ginsenoside Rg2 until 6 and 9 h, respectively, and then gradually decreased until 24 h. By Western blot analysis, it was also revealed that the Ginsenoside 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 Ginsenoside Rg2 for 24 h after UVB exposure, the level of remaining cyclobutane pyrimidine dimers decreased in both Ginsenoside Rg2 concentration- and time-dependent manner. All these results suggest that 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.
    Citation [4]

    Zhongguo Zhong Yao Za Zhi. 2009 May;34(10):1281-4.

    [Study on excretion of ginsenoside Rg2 in rats].[Pubmed: 19673396]
    OBJECTIVE: To determine the Ginsenoside Rg2 and study its excretion in bile, feces and urine of rat. METHOD: Reversed phase high-performance liquid chromatographic (RP-HPLC) method with an ultra-violet detector (UVD) was performed at a detection wavelength of 203 nm and with a Dikma Diamonsil C18 column (4.6 mm x 250 mm, 5 microm), which the mobile phase was consisted of methanol-aq. 4% H3PO4 (65:35), for determination of the Ginsenoside Rg2 in bile, feces and urine after administration of the Ginsenoside Rg2 to rat at a tail vein single dose of 20 mg x kg(-1). RESULT: The HPLC-UVD method fulfilled all the standard requirements of linearity, recovery, precision, and accuracy. After tail vein administration of the Ginsenoside Rg2 to rat, the 5.5 hour cumulative biliary excretion rate and the 24-hour cumulative feces excretion rate of intact Ginsenoside Rg2 were 27.2% and 22.6% of the administered dose, respectively. But intact Ginsenoside Rg2 could not be detected in urine during this experimental period. CONCLUSION: The bile and feces were the main excretion routs of the unchanged form after tail vein administration of the Ginsenoside Rg2 to rat.