Ginsenoside Re - CAS 52286-59-6
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Ginsenoside Re, extracted from the traditional Chinese herb ginseng, responsible for some of the pharmacological functions.
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White powder
Ginsenoside B2; 2-O-(6-deoxy-alpha-L-mannopyranosyl)-(3beta,6alpha,12beta)-20-(beta-D-glucopyranosyloxy)-3,12-dihydroxydammar-24-en-6-yl-beta-D-glucopyranoside;
Soluble in DMSO
Store at -20 °C
Anti-ischemic and anti-arrythmic activities.
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Melting Point:
194 - 205 °C
Canonical SMILES:
1.Ginsenoside Re inhibits pacemaker potentials via adenosine triphosphate-sensitive potassium channels and the cyclic guanosine monophosphate/nitric oxide-dependent pathway in cultured interstitial cells of Cajal from mouse small intestine.
Hong NR1, Park HS1, Ahn TS1, Kim HJ1, Ha KT2, Kim BJ1. J Ginseng Res. 2015 Oct;39(4):314-21. doi: 10.1016/j.jgr.2015.02.004. Epub 2015 Mar 6.
BACKGROUND: Ginseng belongs to the genus Panax. Its main active ingredients are the ginsenosides. Interstitial cells of Cajal (ICCs) are the pacemaker cells of the gastrointestinal (GI) tract. To understand the effects of ginsenoside Re (GRe) on GI motility, the authors investigated its effects on the pacemaker activity of ICCs of the murine small intestine.
2.Protective effects of ginsenoside Re on lipopolysaccharide-induced cardiac dysfunction in mice.
Chen RC1, Wang J1, Yang L2, Sun GB1, Sun XB1. Food Funct. 2016 Apr 14. [Epub ahead of print]
The impaired cardiac function caused by reduced myocardial contractility is a typical manifestation of sepsis/septic shock. Ginsenoside Re (GS-Re) is one of the most abundant ingredients of ginseng. This study was designed to investigate the protective effects of GS-Re on lipopolysaccharide (LPS)-induced septic cardiac dysfunction and inflammatory response in mice. Mice were intragastrically administered with GS-Re (15 mg kg-1) for 1 week before the LPS challenge (10 mg kg-1, i.p.). Cardiac function was evaluated 6 h after LPS induction. GS-Re pretreatment significantly protected against LPS-induced cardiac dysfunction. GS-Re ameliorated the imbalance between iNOS and eNOS, and prevented NF-κB activation and subsequent myocardial inflammatory responses in endotoxemic mice. The effects of GS-Re were closely associated with estrogen receptors (ERs), phosphatidylinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, and the mitogen-activated protein kinase signaling pathway, as characterized by the GS-Re-induced preservation of ERα, ERβ, and phospho-Akt and inhibition of phospho-ERK1/2, phospho-JNK, phospho-P38.
3.YiQiFuMai Powder Injection ameliorates the oxygen-glucose deprivation-induced brain microvascular endothelial barrier dysfunction associated with the NF-κB and ROCK1/MLC signaling pathways.
Cao GS1, Chen HL2, Zhang YY3, Li F4, Liu CH5, Xiang X6, Qi J7, Chai CZ8, Kou JP9, Yu BY10. J Ethnopharmacol. 2016 May 13;183:18-28. doi: 10.1016/j.jep.2016.02.028. Epub 2016 Feb 23.
ETHNOPHARMACOLOGICAL RELEVANCE: YiQiFuMai Powder Injection (YQFM) is a modern preparation derived from Sheng-mai San, a traditional Chinese prescription, widely used for the treatment of cardiovascular and cerebrovascular diseases. However, its potential molecular mechanism remains unclear.
4.Ginsenoside Re Attenuates Neuroinflammation in a Symptomatic ALS Animal Model.
Cai M1, Yang EJ1. Am J Chin Med. 2016 Apr;44(2):401-13. doi: 10.1142/S0192415X16500233.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the progressive loss of upper and lower motor neurons, which cause paralysis and respiratory dysfunction. There is currently no permanently effective drug for patients with ALS. Ginsenoside Re (G-Re), one of the most active ingredients of ginseng, has pharmacological activities that affect a number of targets. To investigate the effects of G-Re on neuroinflammation, we used G-Re (2.5[Formula: see text][Formula: see text]g/g) at the Joksamni acupressure point (ST36) once every other day for one week. To evaluate G-Re function in symptomatic human-superoxide dismutase 1 (hSOD1[Formula: see text] transgenic mice, immunohistochemistry and Western blot analysis were performed with the spinal cord of symptomatic hSOD1(G93A) transgenic mice. Here, we report that G-Re exhibits potent neuroprotective effects against neuroinflammation in a murine model of ALS. G-Re treatment reduced the loss of motor neurons and active-microglia-related expression of Iba-1 in the spinal cord of symptomatic hSOD1(G93A) transgenic mice.
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CAS 52286-59-6 Ginsenoside Re

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