ChemFaces is a professional high-purity natural products manufacturer.
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1. Reference standards
2. Pharmacological research
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More articles cited ChemFaces products.
Arch Toxicol. 2017 Mar 20. Chemistr of plant2016021195Neuropharmacology.2018 Mar 15;J Pharm Biomed Anal. 2017 Jun 5;Sci Rep. 2017 Aug 15;
BMC Complement Altern Med.2016 Jul 13Phytomedicine1 Feb. 2018;Oncotarget. 2016 Aug 19Molecules.2013 Nov 14;18(11):14105-21. Research on Crops.2017, Issue : 3
Biol Pharm Bull. 2018;41(1):65-72.Evid Based Complement Alternat Med. 2017:1583185Br J Pharmacol.2018 Mar;Phytother Res.2018 Jan 29.
Our products had been exported to the following research institutions and universities, And still growing.
Regional Crop Research Institute (Korea)Hamdard University (India)Massachusetts General Hospital (USA)Leibniz-Institut für Pflanzenbi... (Germany)
University of Mysore (India)Korea Institute of Oriental Medi... (Korea)University of Fribourg (Switzerland)Griffith University (Australia)
Subang Jaya Medical Centre (Malaysia)Siksha O Anusandhan University (India)Universidad de Buenos Aires (Argentina)
|| 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. |
||Nrf2 | MEK | ERK | P90RSK|
Notoginsenoside R2 Description
||The roots of Panax notoginseng (Burk.)F.H.Chen
||DMSO, Pyridine, Methanol, Ethanol, etc.
||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: email@example.com
||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.
Recent ChemFaces New Products and Compounds
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.2017.12.030PMID: 29496173
Calculate Dilution Ratios(Only for Reference)
* 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.
|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.
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.