20(S)-Ginsenoside Rh2
Ginsenoside Rh2 has memory-enhancing ,anti-osteoporosis, antitumor, antidiabetic, antiallergic, and anti-inflammatory effects, it potently protects ischemia-reperfusion brain injury, also inhibits prostaglandin-E_2 synthesis in lipopolysaccharide-stimulated RAW264.7 cells. It can inhibit the tendency of apoptosis, and reverse the impaired β-cell growth potential by modulating Akt/Foxo1/PDX-1 signaling pathway and regulating cell cycle proteins; it suppresses RANKL-induced osteoclast differentiation in vitro and in vivo through the regulation of c-Fos and NFATc1 expressions, not excluding the involvement of NF-κB and ERK.
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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.
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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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Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2014 Oct;30(10):1062-6.
[Regulatory effect of ginsenoside Rh2 on HDAC1/2 activity and cyclin in human erythroleukemia K562 cells].[Pubmed:
25270209]
To investigate the effects of the 20(S)-Ginsenoside Rh2 [Rh2(S)]on cell proliferation, histone deacetylase 1 (HDAC1) and HDAC2 activity, and expression of cyclin in human erythroleukemia K562 cells.
METHODS AND RESULTS:
The proliferation of K562 cells was inhibited by 20(S)-Ginsenoside Rh2 (20-80 μmol/L) in dose-and time-dependent manner. FCM analyses revealed that the number of the K562 cells treated with 60 μmol/L 20(S)-Ginsenoside Rh2 was arrested in G0/G1 phase. The apoptosis rates of K562 cells were respectively (8.09±0.86)%, (9.44±0.53)% and (22.80±2.16)% after induced by 20, 40, 60 μmol/L 20(S)-Ginsenoside Rh2, which showed statistically significant difference (P<0.05) compared with the control group (2.63±0.14)%. HDAC activity of the cells treated with 20(S)-Ginsenoside Rh2 (40, 60 μmol/L) was reduced. Western blotting showed that the expressions of HDAC1, HDAC2, cyclin D1 and CDK4 decreased after induced by 20(S)-Ginsenoside Rh2, and p16INK4A, p21 proteins were enhanced significantly.
CONCLUSIONS:
The 20(S)-Ginsenoside Rh2 can inhibit the proliferation of K562 cells and induce its cycle arrest and apoptosis through inhibiting HDAC1 and HDAC2 activity, down-regulating the expression of cyclin D1 and activating p16INK4A and p21.
Biol Pharm Bull. 2014;37(2):248-54.
20S-Ginsenoside Rh2 induces apoptosis in human Leukaemia Reh cells through mitochondrial signaling pathways.[Pubmed:
24492721]
20(S)-Ginsenoside Rh2 (GRh2) and ginsenoside Rg3 (GRg3) are members of the protopanaxadiol family and have been investigated for possible chemopreventive activity. This study explored the biological and apoptotic mechanisms induced by 20(S)-GRh2 in human acute leukaemia line-Reh cells.
METHODS AND RESULTS:
Reh cells were treated with different concentration of 20(S)-Ginsenoside Rh2 in vitro. Cell viability was determined by Cell Counting Kit-8 and Annexin V/7-AAD assays. Mitochondrial membrane potential (MMP) was examined through JC-1 staining. Activation of caspases associated with the mitochondria-mediated apoptosis pathway was determined by Western blot. We observed that survival of Reh cells decreased after exposure to 20(S)-Ginsenoside Rh2 in a concentration-dependent manner. Moreover,20(S)-Ginsenoside Rh2 can induce mitochondria depolarization of Reh cells as evident in the shift in JC-1 fluorescence from red to green. In addition, 20(S)-Ginsenoside Rh2 induced the release of mitochondrial cytochrome c and activation of caspase-9 and caspase-3 in Reh cells.
CONCLUSIONS:
These results indicate that 20(S)-Ginsenoside Rh2 could induce apoptosis through the mitochondrial pathway, demonstrating its potential as a chemotherapeutic agent for leukaemia therapy.
Bioorg Med Chem Lett. 2014 Sep 15;24(18):4407-9.
20(S)-Ginsenoside Rh2 as aldose reductase inhibitor from Panax ginseng.[Pubmed:
25152999]
The root of Panax ginseng C. A. Meyer (Araliaceae) is a well-known herbal medicine in East Asia. The major bioactive metabolites in this root are commonly identified as ginsenosides.
METHODS AND RESULTS:
A series of ginsenosides were determined for in vitro human recombinant aldose reductase. This Letter aims to clarify the structural requirement for aldose reductase inhibition. We discovered that only 20(S)-Ginsenoside Rh2 showed potent against aldose reductase, with an IC50 of 147.3 μM.
CONCLUSIONS:
These results implied that the stereochemistry of the hydroxyl group at C-20 may play an important role in aldose reductase inhibition. An understanding of these requirements is considered necessary in order to develop a new type of aldose reductase inhibitor. Furthermore, P. ginseng might be an important herbal medicine in preventing diabetic complications.
Acta Pharmacol Sin. 2013 Oct;34(10):1349-58.
Pharmacokinetic interactions between 20(S)-ginsenoside Rh2 and the HIV protease inhibitor ritonavir in vitro and in vivo.[Pubmed:
23892274]
20(S)-Ginsenoside Rh2 (Rh2) has shown potent inhibition on P-glycoprotein (P-gp), while most HIV protease inhibitors are both substrates and inhibitors of P-gp and CYP3A4.
The aim of this study was to investigate the potential pharmacokinetic interactions between Rh2 and the HIV protease inhibitor ritonavir.
METHODS AND RESULTS:
20(S)-Ginsenoside Rh2 (10 μmol/L) significantly increased the accumulation and inhibited the efflux of ritonavir in Caco-2 and MDCK-MDR1 cells, as verapamil did. But 20(S)-Ginsenoside Rh2 did not significantly alter ritonavir accumulation or transport in MDCK-WT cells. Intravenous 20(S)-Ginsenoside Rh2 significantly increased the plasma exposure of ritonavir while reducing its excretion in the bile, and oral verapamil or GF120918 also increased plasma exposure of ritonavir but without changing its excretion in the bile. Interestingly, oral 20(S)-Ginsenoside Rh2 at both doses did not significantly change the plasma profile of ritonavir. Moreover, oral 20(S)-Ginsenoside Rh2 (25 mg/kg) significantly elevated the ritonavir concentration in the hepatic portal vein, and markedly increased its urinary excretion and tissue distribution, which might counteract the elevated absorption of ritonavir.
CONCLUSIONS:
20(S)-Ginsenoside Rh2 inhibits the efflux of ritonavir through P-gp in vitro. The effects of 20(S)-Ginsenoside Rh2 on ritonavir exposure in vivo depend on the administration route of 20(S)-Ginsenoside Rh2: intravenous, but not oral, administration of 20(S)-Ginsenoside Rh2 significantly increased the plasma exposure of ritonavir.
