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    Notoginsenoside R2
    Information
    CAS No. 80418-25-3 Price $218 / 20mg
    Catalog No.CFN92364Purity>=98%
    Molecular Weight771.0Type of CompoundTriterpenoids
    FormulaC41H70O13Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Notoginsenoside R2 has neuroprotection against 6-OHDA-induced neurotoxicity, is associated with Notoginsenoside R2-mediated P90RSK and Nrf2 activation through MEK1/2-ERK1/2 pathways.
    Targets: Nrf2 | MEK | ERK | P90RSK
    Notoginsenoside R2 Description
    Source: The roots of Panax notoginseng (Burk.)F.H.Chen
    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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    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.

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    PMID: 29230013

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

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

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    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 1.297 mL 6.4851 mL 12.9702 mL 25.9403 mL 32.4254 mL
    5 mM 0.2594 mL 1.297 mL 2.594 mL 5.1881 mL 6.4851 mL
    10 mM 0.1297 mL 0.6485 mL 1.297 mL 2.594 mL 3.2425 mL
    50 mM 0.0259 mL 0.1297 mL 0.2594 mL 0.5188 mL 0.6485 mL
    100 mM 0.013 mL 0.0649 mL 0.1297 mL 0.2594 mL 0.3243 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.
    Protocol
    Kinase Assay:
    Evid Based Complement Alternat Med. 2013;2013:971712.
    P90RSK and Nrf2 Activation via MEK1/2-ERK1/2 Pathways Mediated by Notoginsenoside R2 to Prevent 6-Hydroxydopamine-Induced Apoptotic Death in SH-SY5Y Cells.[Pubmed: 24159358]
    6-Hydroxydopamine (6-OHDA) is known to contribute to neuronal death in Parkinson's disease.
    METHODS AND RESULTS:
    In this study, we found that the preincubation of SH-SY5Y cells for 24 h with 20  μ M Notoginsenoside R2 (NGR2), which is a newly isolated notoginsenoside from Panax notoginseng, showed neuroprotective effects against 6-OHDA-induced oxidative stress and apoptosis. NGR2 incubation successively resulted in the activation of P90RSK, inactivation of BAD, and inhibition of 6-OHDA-induced mitochondrial membrane depolarization, thus preventing the mitochondrial apoptosis pathway. NGR2 incubation also led to the activation of Nrf2 and subsequent activity enhancement of phase II detoxifying enzymes, thus suppressing 6-OHDA-induced oxidative stress, and these effects could be removed by Nrf2 siRNA. We also found that the upstream activators of P90RSK and Nrf2 were the MEK1/2-ERK1/2 pathways but not the JNK, P38, or PI3K/Akt pathways. Interestingly, NGR2 incubation could also activate MEK1/2 and ERK1/2. Most importantly, NGR2-mediated P90RSK and Nrf2 activation, respective downstream target activation, and neuroprotection were reversed by the genetic silencing of MEK1/2 and ERK1/2 by using siRNA and PD98059 application.
    CONCLUSIONS:
    These results suggested that the neuroprotection elicited by NGR2 against 6-OHDA-induced neurotoxicity was associated with NGR2-mediated P90RSK and Nrf2 activation through MEK1/2-ERK1/2 pathways.