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    Ginsenoside Rg1
    CAS No. 22427-39-0 Price $40 / 20mg
    Catalog No.CFN99967Purity>=98%
    Molecular Weight801.01Type of CompoundTriterpenoids
    FormulaC42H72O14Physical DescriptionWhite powder
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  • Biological Activity
    Description: Ginsenoside Rg1 has antiaging, anti-platelet activation, promotion of wound healing, and neuroprotective effects, it has protective effect against Aβ25-35-induced toxicity in PC12 cells,might be through the insulin-like growth factor-I receptor (IGF-IR) and estrogen receptor (ER)signaling pathways. Ginsenoside Rg1 is a desirable agent for enhancing CD4+ T-cell activity, as well as the correction of Th1-dominant pathological disorders, which by increasing Th2 specific cytokine secretion and by repressing Th1 specific cytokine production. It increased the expression of the vascular endothelial growth factor (VEGF) mRNA and reduced ERK pathway, expression of transforming growth factor beta (TGF-β) mRNA.
    Targets: ERK | Akt | MEK | PI3K | Bcl-2/Bax | Beta Amyloid | VEGFR | TGF-β/Smad | IFN-γ | IL Receptor | gp120/CD4 | IGF-IR | Estrogen receptor
    In vitro:
    Acta Pharmacol Sin. 2009 Mar;30(3):299-306.
    Ginsenoside Rg1 promotes endothelial progenitor cell migration and proliferation.[Pubmed: 19262553]
    To investigate the effect of Ginsenoside Rg1 on the migration, adhesion, proliferation, and VEGF expression of endothelial progenitor cells (EPCs).
    EPCs were isolated from human peripheral blood and incubated with different concentrations of Ginsenoside Rg1 (0.1, 0.5, 1.0, and 5.0 micromol/L) and vehicle controls. EPC migration was detected with a modified Boyden chamber assay. EPC adhesion was determined by counting adherent cells on fibronectin-coated culture dishes. EPC proliferation was analyzed with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In vitro vasculogenesis was assayed using an in vitro vasculogenesis detection kit. A VEGF-ELISA kit was used to measure the amount of VEGF protein in the cell culture medium. Ginsenoside Rg1 promoted EPC adhesion, proliferation, migration and in vitro vasculogenesis in a dose- and time-dependent manner. Cell cycle analysis showed that 5.0 micromol/L of Ginsenoside Rg1 significantly increased the EPC proliferative phase (S phase) and decreased the resting phase (G(0)/G(1) phase). Ginsenoside Rg1 increased vascular endothelial growth factor production.
    The results indicate that Ginsenoside Rg1 promotes proliferation, migration, adhesion and in vitro.
    Int Immunopharmacol. 2004 Feb;4(2):235-44.
    Ginsenoside Rg1 enhances CD4(+) T-cell activities and modulates Th1/Th2 differentiation.[Pubmed: 14996415]
    Panax ginseng is commonly used as a tonic medicine in Asian countries such as Korea, China, and Japan. It has been reported that Ginsenoside Rg1 in P. ginseng increases the proportion of T helper (Th) cells among the total number of T cells and promotes IL-2 gene expression in murine splenocytes. This implies that Ginsenoside Rg1 increases the immune activity of CD4(+) T cells, however, the exact mechanism remains unknown.
    The present study elucidated the direct effect of Rg1 on helper T-cell activities and on Th1/Th2 lineage development. The results demonstrated that Ginsenoside Rg1 had no mitogenic effects on unstimulated CD4(+) T cells, but augmented CD4(+) T-cell proliferation upon activation with anti-CD3/anti-CD28 antibodies in a dose-dependent manner. Rg1 also enhanced the expression of cell surface protein CD69 on CD4(+) T cells. In Th0 condition, Ginsenoside Rg1 increases the expression of IL-2 mRNA, and enhances the expression of IL-4 mRNA on CD4(+) T cells, suggesting that Rg1 prefers to induce Th2 lineage development. In addition, Ginsenoside Rg1 increases IL-4 secretion in CD4(+) T cells under Th2 skewed condition, while decreasing IFN-gamma secretion of cells in Th1 polarizing condition. Thus, Rg1 enhances Th2 lineage development from the naïve CD4(+) T cell both by increasing Th2 specific cytokine secretion and by repressing Th1 specific cytokine production.
    Therefore, these results suggest that Ginsenoside Rg1 is a desirable agent for enhancing CD4(+) T-cell activity, as well as the correction of Th1-dominant pathological disorders.
    In vivo:
    J Gerontol A Biol Sci Med Sci. 2014 Mar;69(3):282-94.
    Long-term ginsenoside Rg1 supplementation improves age-related cognitive decline by promoting synaptic plasticity associated protein expression in C57BL/6J mice.[Pubmed: 23833204 ]
    In aging individuals, age-related cognitive decline is the most common cause of memory impairment. Among the remedies, Ginsenoside Rg1, a major active component of ginseng, is often recommended for its antiaging effects. However, its role in improving cognitive decline during normal aging remains unknown and its molecular mechanism partially understood.
    This study employed a scheme of Rg1 supplementation for female C57BL/6J mice, which started at the age of 12 months and ended at 24 months, to investigate the effects of Rg1 supplementation on the cognitive performance. We found that Rg1 supplementation improved the performance of aged mice in behavior test and significantly upregulated the expression of synaptic plasticity-associated proteins in hippocampus, including synaptophysin, N-methyl-D-aspartate receptor subunit 1, postsynaptic density-95, and calcium/calmodulin-dependent protein kinase II alpha, via promoting mammalian target of rapamycin pathway activation.
    These data provide further support for Rg1 treatment of cognitive degeneration during aging.
    Thromb Res. 2014 Jan;133(1):57-65.
    Ginsenoside Rg1 inhibits platelet activation and arterial thrombosis.[Pubmed: 24196231 ]
    Derived from the root of Panax ginseng C.A.Mey, Panax notoginsenosides (PNS) is a widely used herbal medicine to treat atherothrombotic diseases in Asian medicine. Ginsenoside Rg1 is one of the main compounds responsible for the pharmaceutical actions of PNS. As platelets play pivotal roles in atherothrombogenesis, we therefore studied the effect of Rg1 on platelet activation and its underlying mechanisms.
    Human platelets are obtained from healthy subjects. Platelet activation and the inhibition of Rg1 were assessed by Born aggregometer, flow cytmetry, flow chamber and western blot. The in vivo thrombosis model was induced by 10% FeCl3 on mesenteric arterioles of wild type B57/b6 mice. Rg1 significantly inhibited platelet aggregation induced by thrombin, ADP, collagen and U46619, e.g., aggregation rate stimulated by 0.1UmL(-1) thrombin was decreased 46% by Rg1. Rg1 also reduced thrombin (0.1UmL(-1))-enhanced fibrinogen binding and P-selectin expression of single platelet by 81% and 66%, respectively. Rg1 affected αIIbβ3-mediated outside-in signaling as demonstrated by diminished platelet spreading on immobilized fibrinogen. Rg1 also decreased the rate of clot retraction in platelet rich plasma. Furthermore, Rg1 decreased platelet adhesion on collagen surface under a shear rate correlated to the arterial flow (1000s(-1)) by approximately 70%. Western blot showed that Rg1 potently inhibited ERK phosphrylation. The in vitro findings were further evaluated in the mouse model of in vivo arterial thrombosis, and Rg1 was found to prolong the mesenteric arterial occlusion time (34.9±4.1min without and 64.3±4.9min with Rg1; p<0.01).
    Rg1 inhibits platelet activation via the inhibition of ERK pathway, and attenuates arterial thrombus formation in vivo.
    Ginsenoside Rg1 Description
    Source: The roots of Panax ginseng C. A. Mey.
    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

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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 1.2484 mL 6.2421 mL 12.4842 mL 24.9685 mL 31.2106 mL
    5 mM 0.2497 mL 1.2484 mL 2.4968 mL 4.9937 mL 6.2421 mL
    10 mM 0.1248 mL 0.6242 mL 1.2484 mL 2.4968 mL 3.1211 mL
    50 mM 0.025 mL 0.1248 mL 0.2497 mL 0.4994 mL 0.6242 mL
    100 mM 0.0125 mL 0.0624 mL 0.1248 mL 0.2497 mL 0.3121 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.
    Cell Research:
    Neurochem Int. 2013 Jan;62(1):92-102.
    Ginsenoside Rg1 facilitates neural differentiation of mouse embryonic stem cells via GR-dependent signaling pathway.[Pubmed: 23063465]
    Ginsenoside Rg1, a steroidal saponin of high abundance in ginseng, possesses the neuroprotective effects.
    In this study, we tried to explore the effect of Rg1 on promoting differentiation of mouse embryonic stem (ES) cells towards the neuronal lineage and its potential role involved in glucocorticoid receptor (GR) activation. Rg1 treatment induced a remarkable increase in the population of neuron-like cells in a time-dependent manner. More than 80% of Rg1-treated embryoid bodies (EBs) differentiated into neuron-like cells on d 8+10. Furthermore, the gradually increased protein expression of neurofilament (NEFM) and β-tubulin III (a neuronal specific protein) was determined. GR expression gradually increased during the differentiation course. RU486, an antagonist of GR, could efficiently block the neurogenesis-promoting activity of Rg1. On the other side, Rg1 stimulated the phosphorylation of ERK1/2 and Akt at different time points through GR activation-dependent mechanisms. Treatment of both U0126 (an inhibitor of MEK) and LY294002 (an inhibitor of PI3 K), hampered the neuronal differentiation induced by Rg1. Meantime, U0126 further decreased Rg1-induced p-Akt expression.
    In conclusion, Rg1 possesses the effects on inducing differentiation of mouse ES cells into neurons in vitro via the GR-MEK-ERK1/2-PI3 K-Akt signaling pathway.
    Neurochem Int. 2013 Jun;62(8):1065-71.
    Involvement of IGF-I receptor and estrogen receptor pathways in the protective effects of ginsenoside Rg1 against Aβ₂₅₋₃₅-induced toxicity in PC12 cells.[Pubmed: 23603302 ]
    Ginsenoside Rg1 is the main pharmacologically active compound of ginsenosides and has demonstrated pharmacological effects in the cardiovascular system, central nervous system and immune system. The involvement of insulin-like growth factor-I receptor (IGF-IR)-dependent pathway and estrogen receptor (ER)-dependent pathway in the biological effect of Ginsenoside Rg1 have been demonstrated in our previous study. The present study tested the hypothesis that the protective effects of Rg1 against Aβ25-35-induced toxicity involved activation of the IGF-IR and ER signaling pathways in PC12 cells.
    Treatment with Aβ25-35 decreased the cell viability in a dose-dependent manner in PC12 cells. Rg1 pretreatment resulted in an enhancement of survival and the maximum protection occurred at the concentration of 1μM. Co-treatment with IGF-IR antagonist JB-1 or ER antagonist ICI182,780 could completely block the protective effect of Rg1. The decreased Bcl-2 mRNA expression induced by Aβ25-35 could be restored by Rg1 pretreatment. Rg1 pretreatment could also restore the decreased mitochondrial membrane potential induced by Aβ25-35 and these effects could be completely blocked by JB-1 or ICI182,780. In addition, Rg1 treatment alone could significantly increase the phosphorylation level of MEK and ERK in a time-dependent manner and the functional transactivation of ERα in PC12 cells. The functional transactivation of ERα by Rg1 could be completely blocked by JB-1 or ICI182,780.
    Taken together, our results suggest that IGF-IR and ER signaling pathways might be involved in the protective effect of Rg1 against Aβ25-35-induced toxicity in PC12 cells.
    Animal Research:
    J Korean Soc Food Sci Nutr,2010, 39(10):437-45.
    Healing Effects of Ginsenoside Rg1 on Experimental Open Wound in Rat.[Reference: WebLink]
    This study was performed to investigate the effect of Ginsenoside Rg1 treatment on wound healing using SD rats by generating four full-thickness skin wounds on the dorsum.
    In the Rg1-treated groups (5,000 and 10,000 ppm), area of wounds and macroscopic inflammatory signs were significantly decreased compared to control group throughout the experimental period in a concentration dependent manner. Histological appearance after 20 days of treatment with Rg1 revealed the formation of epithelial layer, hair follicles and progressive angiogenesis and an increase in collagen and granulation as compared to control group. Rg1 treatment resulted in the increased expression of the vascular endothelial growth factor (VEGF) mRNA and reduced expression of transforming growth factor beta (TGF-β) mRNA in wounded skin compared to control group. The expression levels of VEGF and TGF-β mRNA in the Rg1-treated groups were similar to those of Fucidin® ointment-treated group.
    These results suggested that Rg1 should be helpful for the promotion of wound healing.