Home Neuronal Signaling Beta Amyloid inhibitor Ginsenoside Re

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Ginsenoside Re Beta Amyloid inhibitor

Cat.No.S3811

Ginsenoside Re (Ginsenoside B2, Panaxoside Re, Sanchinoside Re, Chikusetsusaponin Ivc), an extract from Panax notoginseng, is a major ginsenoside in ginseng and belongs to 20(S)-protopanaxatriol group. It has diverse in vitro and in vivo effects, including vasorelaxant, antioxidant, antihyperlipidemic, and angiogenic actions. This compound decreases the β-amyloid protein (Aβ). It plays a role in antiinflammation through inhibition of JNK and NF-κB.
Ginsenoside Re Beta Amyloid inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 947.15

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Quality Control

Batch: Purity: 99.14%
99.14

Solubility

In vitro
Batch:

DMSO : 100 mg/mL (105.57 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 20 mg/mL

Water : Insoluble

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In vivo
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Chemical Information, Storage & Stability

Molecular Weight 947.15 Formula

C48H82O18

 Storage (From the date of receipt)
CAS No. 52286-59-6 Download SDF Storage of Stock Solutions

Synonyms Panaxoside Re, Sanchinoside Re, Chikusetsusaponin Ivc Smiles CC1C(C(C(C(O1)OC2C(C(C(OC2OC3CC4(C(CC(C5C4(CCC5C(C)(CCC=C(C)C)OC6C(C(C(C(O6)CO)O)O)O)C)O)C7(C3C(C(CC7)O)(C)C)C)C)CO)O)O)O)O)O

Mechanism of Action

Targets/IC50/Ki
Aβ
JNK
NF-κB
In vitro

Ginsenoside Re inhibits Ca2+ accumulation in mitochondria during cardiac ischemia/reperfusion, which is attributable to nitric oxide (NO)-induced Ca2+ channel inhibition and K+ channel activation in cardiac myocytes. This compound activates endothelial NO synthase (eNOS) to release NO, resulting in activation of the slowly activating delayed rectifier K+ current. However, it does not stimulate proliferation of androgen-responsive LNCaP cells and estrogen-responsive MCF-7 cells, implying that this chemical does not activate a genomic pathway of sex hormone receptors. It induces phosphorylation of Akt in cardiomyocytes in a concentration-dependent manner. This compound is a partial agonist of the AR, ERα, and PR. It is a partial antagonist, but not an agonist, of the genomic pathway of AR or ERα.
In vivo

The absorption of Ginsenoside Re is fast in gastrointestinal tract. This compound may be metabolized mainly to Rh1 and F1 by intestinal microflora before absorption into blood; and it is quickly cleared from the body. In cardiovascular system, this chemical possesses negative effects on cardiac contractility and autorhythmicity, anti-arrhythmic and anti-ischemic effects, angiogenic regeneration activities and cardiac electrophysiological functions. It reaches peak concentration in plasma within about 45 minutes after oral administration of total panax notoginsenoside (TPNG) powder in rats, suggesting a rapid absorption in gastrointestinal tract. The absolute bioavailability of this compound is 7.06%. In pharmacokinetic study using ICR mice, the time to reach the peak plasma concentration after oral administration is 0.4 ± 0.2 hour and the oral bioavailability is 0.19-0.28%. This chemical is rapidly cleared from the body within 0.2 ± 0.03 hour for male mice and 0.5 ± 0.08 hour for female mice after intravenous administration. Its administration in ob/ob mice significantly reduces fasting blood glucose levels, improves glucose tolerance and systemic insulin sensitivity without affecting body weight. These events are mediated, at least in part, by the changes in skeletal muscle gene expression.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/27840193/
  • [5] https://pubmed.ncbi.nlm.nih.gov/17885204/

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