Ginsenoside Rf CAS NO.52286-58-5

Hubei CuiRan Biotechnology Co., Ltd is a leading company in the research, development, manufacture and marketing of High Quality Phytochemicals and Extracts(especially Active Ingredients from Traditional Chinese Medicine，Traditional Chinese Medicine), Natural Active Pharmaceutical Ingredients worldwide. From small quantities for R&D or reference standard, to large quantities for customizing or manufacturing, Biopurify emphasizes on consistent and reliable services for his customers. 
With excellent quality products and good service, we have clients from more than dozens countries and regions, and we pride ourselves in providing our customers with a total satisfaction experiences.
We are doing our best to be your reliable partner for high quality Phytochemicals and Reference Standards from china.
 
Our main services:
A. Supply active ingredients and reference standards ofTraditional Chinese Medicine, from mgs to kgs scale.
B. Custom extraction and purification, target Herb Active Ingredients
C. Custom synthesis and semi-synthesis for Natural Active Ingredients
D. CR, CM and PD services from lab scale, pilot scale to commercial scale(GMP is also available)
E.Traditional Chinese Medicine compounds library
 

1.Provide traditional Chinese medicine reference materials and natural active ingredients;
2.More than 2200 compounds are available for selection, continuously building high-quality natural product libraries for drug research and development;
3.Provide various screening libraries and more inhibitor products;
4.Provide separation and structural determination of natural products;
5.Laboratory scale pilot to commercial scale collaborative research and process development services.More than 180 experiences in phytochemistry (still increasing)
Each product has passed very strict testing (NMR/MS/HPLC)
Agents from many countries

General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging：1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition：Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Chemical Properties of Ginsenoside Rf

Source of Ginsenoside Rf

The roots of Panax ginseng C. A. Mey.

Biological Activity of Ginsenoside Rf

Protocol of Ginsenoside Rf

Preparing Stock Solutions of Ginsenoside Rf

References on Ginsenoside Rf

Suppression of MAPKs/NF-kappaB Activation Induces Intestinal Anti-Inflammatory Action of Ginsenoside Rf in HT-29 and RAW264.7 Cells.[Pubmed:27224660]

Immunol Invest. 2016 Jul;45(5):439-49.

This study investigated the intestinal anti-inflammatory action of Ginsenoside Rf in inflammatory bowel disease (IBD). IBD is a chronic inflammatory disease that affects the intestinal tract. It is associated with elevated levels of various inflammatory mediators, including interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO), and reactive oxygen species (ROS). Ginsenosides, the main active constituents of ginseng, have been reported to exert potent therapeutic effects against diverse diseases. However, Ginsenoside Rf treatment for inflammation has not yet been examined. In this study, we evaluated the inhibitory effect of Ginsenoside Rf on the inflammatory mediators downstream of p38/NF-kB activation on TNF-alpha-stimulated intestinal epithelial cells (HT-29) and mouse macrophage cells (RAW264.7). Our results showed that Ginsenoside Rf significantly reduced the production of IL-1beta, IL-6, TNF-alpha, NO, and ROS, which are most highly activated in IBD. In addition, Ginsenoside Rf significantly suppressed TNF-alpha/LPS-induced NF-kappaB transcriptional activity. These results suggest that Ginsenoside Rf contains a compound that has potent intestinal anti-inflammatory effects that could be used to treat diseases such as IBD.

Functional expression of a novel ginsenoside Rf binding protein from rat brain mRNA in Xenopus laevis oocytes.[Pubmed:11901233]

Mol Pharmacol. 2002 Apr;61(4):928-35.

We have shown that Ginsenoside Rf (Rf) regulates voltage-dependent Ca(2+) channels through pertussis toxin (PTX)-sensitive G proteins in rat sensory neurons. These results suggest that Rf can act through a novel G protein-linked receptor in the nervous system. In the present study, we further examined the effect of Rf on G protein-coupled inwardly rectifying K(+) (GIRK) channels after coexpression with size-fractionated rat brain mRNA and GIRK1 and GIRK4 (GIRK1/4) channel cRNAs in Xenopus laevis oocytes using two-electrode voltage-clamp techniques. We found that Rf activated GIRK channel in a dose-dependent and reversible manner after coexpression with subfractions of rat brain mRNA and GIRK1/4 channel cRNAs. This Rf-evoked current was blocked by Ba(2+), a potassium channel blocker. The size of rat brain mRNA responding to Rf was about 6 to 7 kilobases. However, Rf did not evoke GIRK current after injection with this subfraction of rat brain mRNA or GIRK1/4 channel cRNAs alone. Other ginsenosides, such as Rb(1) and Rg(1), evoked only slight induction of GIRK currents after coexpression with the subfraction of rat brain mRNA and GIRK1/4 channel cRNAs. Acetylcholine and serotonin almost did not induce GIRK currents after coexpression with the subfraction of rat brain mRNA and GIRK1/4 channel cRNAs. Rf-evoked GIRK currents were not altered by PTX pretreatment but were suppressed by intracellularly injected guanosine-5'-(2-O-thio) diphosphate, a nonhydrolyzable GDP analog. These results indicate that Rf activates GIRK channel through an unidentified G protein-coupled receptor in rat brain and that this receptor can be cloned by the expression method demonstrated here.

Induction of G2/M phase cell cycle arrest and apoptosis by ginsenoside Rf in human osteosarcoma MG63 cells through the mitochondrial pathway.[Pubmed:24173574]

Oncol Rep. 2014 Jan;31(1):305-13.

Ginsenosides, extracted from the traditional Chinese herb ginseng, are a series of novel natural anticancer products known for their favorable safety and efficacy pro fi les. The present study aimed to investigate the cytotoxicity of Ginsenoside Rf to human osteosarcoma cells and to explore the anticancer molecular mechanisms of Ginsenoside Rf. Five human osteosarcoma cell lines (MG-63, OS732, U-2OS, HOS and SAOS-2) were employed to investigate the cytotoxicity of Ginsenoside Rf by MTT and colony forming assays. After treatment with Ginsenoside Rf, MG-63 cells which were the most sensitive to Ginsenoside Rf, were subjected to flow cytometry to detect cell cycle distribution and apoptosis, and nuclear morphological changes were visualized by Hoechst 33258 staining. Caspase-3, -8 and -9 activities were also evaluated. The expression of cell cycle markers including cyclin B1 and Cdk1 was detected by RT-PCR and western blotting. The expression of apoptotic genes Bcl-2 and Bax and the release of cytochrome c were also examined by western blotting. Change in the mitochondrial membrane potential was observed by JC-1 staining in situ. Our results demonstrated that the cytotoxicity of Ginsenoside Rf to these human osteosarcoma cell lines was dose-dependent, and the MG-63 cells were the most sensitive to exposure to Ginsenoside Rf. Additionally, Ginsenoside Rf induced G2/M phase cell cycle arrest and apoptosis in MG-63 cells. Furthermore, we observed upregulation of Bax and downregulation of Bcl-2, Cdk1 and cyclin B1, the activation of caspase-3 and -9 and the release of cytochrome c in MG-63 cells following treatment with Ginsenoside Rf. Our findings demonstrated that Ginsenoside Rf induces G2/M phase cell cycle arrest and apoptosis in human osteosarcoma MG-63 cells through the mitochondrial pathway, suggesting that Ginsenoside Rf, as an effective natural product, may have a therapeutic effect on human osteosarcoma.

Ginsenoside Rf potentiates U-50,488H-induced analgesia and inhibits tolerance to its analgesia in mice.[Pubmed:12479975]

Life Sci. 2003 Jan 3;72(7):759-68.

In the present study, the effect of Ginsenoside Rf (Rf), a trace component of Panax ginseng on U-50,488H (U50), a selective kappa opioid-induced analgesia and its tolerance to analgesia was studied using the mice tail-flick test. In addition, the possible mechanism by which Rf may affect U50-induced analgesia was investigated. Intraperitoneal administration of U50 (40 mg/kg) produced analgesia. Rf (10(-14)-10(-10) mg/kg) on co treatment dose-dependently potentiated the U50 (40 mg/kg)-induced analgesia. Rf (10(-12)-10(-2) mg/ml) did not alter the binding of [3H] naloxone, a opioid ligand and [3H]PN200-110, a dihydropyridine ligand to mice whole brain membrane. Twice daily administration of U50 (40 mg/kg) for six days induced tolerance to its analgesia. Chronic treatment (day 4-day 6) of Rf (10(-14)-10(-10) mg/kg) to U50-tolerant mice, dose-dependently inhibited the tolerance. The inhibition of tolerance to U50-induced analgesia by Rf was not altered by flumazenil (0.1 mg/kg), a benzodiazepine receptor antagonist and picrotoxin (1 mg/kg), a GABA(A)-gated chloride channel blocker on chronic treatment. In conclusion, these findings for the first time demonstrated that Ginsenoside Rf potentiates U50-induced analgesia, inhibits tolerance to its analgesia, and suggests that Rf affects U50-induced analgesia via non-opioid, non-dihydropyridine-sensitive Ca(+2) and non-benzodiazepine-GABA(A)ergic mechanisms in mice.

Induction of CYP3A4 and MDR1 gene expression by baicalin, baicalein, chlorogenic acid, and ginsenoside Rf through constitutive androstane receptor- and pregnane X receptor-mediated pathways.[Pubmed:20580705]

Eur J Pharmacol. 2010 Aug 25;640(1-3):46-54.

The herbal products baicalin, baicalein, chlorogenic acid, and Ginsenoside Rf have multiple pharmacological effects and are extensively used in alternative and/or complementary therapies. The present study investigated whether baicalin, baicalein, chlorogenic acid, and Ginsenoside Rf induced the expression of the cytochrome P450 3A4 (CYP3A4) and multi-drug resistance 1 (MDR1) genes through the pregnane X receptor and constitutive androstane receptor pathways. Real time PCR, western blotting, and a luminescent assay were used to assess the induction of gene expression and activity of CYP3A4 and MDR1 by the test compounds. The interactions of baicalein/chlorogenic acid/Ginsenoside Rf with constitutive androstane receptor and pregnane X receptor were evaluated using luciferase reporter and gel shift assays. Baicalein induced the expression of CYP3A4 and MDR1 mRNA by activating pregnane X receptor and constitutive androstane receptor. Chlorogenic acid and Ginsenoside Rf showed a relatively weak effect on CYP3A4 promoter activation only in HepG2 cells cotransfected with constitutive androstane receptor and demonstrated no effects on MDR1 via either the constitutive androstane receptor or pregnane X receptor pathway. Baicalin had no effect on either CYP3A4 or MDR1 gene expression. In conclusion, baicalein has the potential to up-regulate CYP3A4 and MDR1 through the direct activation of the constitutive androstane receptor and pregnane X receptor pathways. Chlorogenic acid and Ginsenoside Rf only induced constitutive androstane receptor-mediated CYP3A4 expression.

Ginsenoside Rf, a trace component of ginseng root, produces antinociception in mice.[Pubmed:9593902]

Brain Res. 1998 May 11;792(2):218-28.

Ginseng root, a traditional oriental medicine, contains more than a dozen biologically active saponins called ginsenosides, including one present in only trace amounts called ginsenoside-Rf (Rf). Previously, we showed that Rf inhibits Ca2+ channels in mammalian sensory neurons through a mechanism requiring G-proteins, whereas a variety of other ginsenosides were relatively ineffective. Since inhibition of Ca2+ channels in sensory neurons contributes to antinociception by opioids, we tested for analgesic actions of Rf. We find dose-dependent antinociception by systemic administration of Rf in mice using two separate assays of tonic pain: in the acetic acid abdominal constriction test, the ED50 was 56+/-9 mg/kg, a concentration similar to those reported for aspirin and acetaminophen in the same assay; in the tonic phase of the biphasic formalin test, the ED50 was 129+/-32 mg/kg. Rf failed to affect nociception measured in three assays of acute pain: the acute phase of the formalin test, and the thermal (49 degrees C) tail-flick and increasing-temperature (3 degrees C/min) hot-plate tests. The simplest explanation is that Rf inhibits tonic pain without affecting acute pain, but other possibilities exist. Seeking a cellular explanation for the effect, we tested whether Rf suppresses Ca2+ channels on identified nociceptors. Inhibition was seen on large, but not small, nociceptors. This is inconsistent with a selective effect on tonic pain, so it seems unlikely that Ca2+ channel inhibition on primary sensory neurons can fully explain the behavioral antinociception we have demonstrated for Rf.

Description

Ginsenoside Rf is a trace component of ginseng root. Ginsenoside Rf inhibits N-type Ca2+ channel.