White crystalline powder
root of Panax ginseng C. A. Mey.
β-D-Glucopyranoside, (3β,12β)-20-(β-D-glucopyranosyloxy)-12-hydroxydammar-24-en-3-yl/20(S)-Ginsenoside-F2/(3β,12β)-20-(β-D-Glucopyranosyloxy)-12-hydroxydammar-24-en-3-yl β-D-glucopyranoside/GINSENOSIDE F2/GinsenosideF2
871.5±65.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:62025-49-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Recently, the allergenicity of ginsenosides, as main active components in ginseng, has attracted much attention. Ginsenoside Rb1 and Rd. have been reported to induce anaphylactoid reaction. In this study, the allergenicity of a series of 20(S)-protopanaxadiol (PPD) type ginsenosides, including Rb1, Rd., F2, Compound K and 20(S)-PPD, was evaluated in rat basophilic leukemia 2H3 (RBL2H3) cells. As a result, 20(S)-PPD had no effect on the mast cell degranulation, but other components showed anaphylactoid potential to different extent. The allergenicity was stronger and stronger according to the order “Rb1, Rd., F2, Compound K”. Then, F2 was further verified in RBL-2H3 cells, mouse peritoneal mast cells (MPMCs), Laboratory of Allergic Disease 2 (LAD2) human mast cells in vitro and mice in vivo. Results showed that F2 could induce a significant increase of histamine release and translocation of phosphatidylserine in RBL-2H3 cells. F2 also increased β-hexosaminidase release and the intracellular Ca2+ concentration of MPMCs and LAD2 cells. In addition, histamine level in serum of mice was elevated dose-dependently. Our study revealed the potential structure-allergenicity relationship of 20(S)-PPD type ginsenosides and first verified the allergenicity of ginsenoside F2. This study could guide the establishment of quality standards for safe application of ginsenoside-containing preparations.
Copyright © 2017. Published by Elsevier B.V.
20(S)-protopanaxadiol type ginsenoside; Anaphylactoid reaction; Ginsenoside F2; Mast cell degranulation
Ginsenoside F2 induces the release of mediators associated with Anaphylactoid reactions.
Wang L1, Zhang F2, Cao Z2, Xiao Y3, Li S2, Yu B4, Qi J5.
To investigate the inhibitive effects of ginsenoside F2 on oxidative stress in human embryonic kidney cells(HEK-293).
Hydrogen peroxide induced oxidative stress of HEK-293 cell was used as the research object. HEK-293 cells were pretreated with different concentrations of ginsenoside F2(1.25, 5, 20 μmol/L). Cell viability was measured by MTS assay. Malondialchehyche(MDA) level and activities of antioxidant enzymes(superoxide dismutase SOD, glutathione peroxidase GSH-Px, catalase CAT) were measured by corresponding assay kits. DCFH-DA fluorescent probe assay was used to measure the level of intracellular reactive oxygen species(ROS). Quantitative real-time PCR and Western blot were used to detect the expression of nuclear factor erythroid 2-related factor 2(Nrf2) and kelch-like ECH associated protein 1(Keap1).
After treated with 1.25, 5, 20 μmol/L ginsenoside F2, no cytotoxic or proliferative effects were shown on normal HEK-293 cells. After pretreatment with ginsenoside F2, the cell viability was significantly higher than that of the injury group(P<0.05)and increased in a concentration-dependent manner. The fluorescence intensity of oxidative DCF in injured group was significantly increased compared with control group(P<0.05). The fluorescence intensity of cells which pretreated with different concentrations of ginsenoside F2 was gradually weakened(P<0.05). The ROS content of control group was chosen as the standard, and the relative amount of ROS pretreated by ginsenoside F2 decreased in a concentration-dependent manner. After pretreatment of ginsenoside F2, the MDA levels decreased in a concentration-dependent manner and the activities of SOD and GSH-Px were significantly higher than those of the injured group(P<0.05). The activity of CAT was significantly increased with pretreatment of higher concentrations of ginsenoside F2(P<0.05). Furthermore, ginsenoside F2 significantly enhanced the protein and mRNA expressions of Nrf2 and reduced the expressions of Keap1 in a dose-dependent manner(P<0.05).
Ginsenoside F2 protect HEK-293 cells against H_2O_2-induced oxidative stress through reducing intracellular ROS and MDA, as well as activating Nrf2/Keap1 signaling pathway and antioxidant enzymes.
ginsenoside F2; nuclear factor erythroid 2-related factor 2(Nrf2); oxidative stress; signal pathway
[Protective effects of ginsenoside F2 on hydrogen peroxide induced cell injury].
Liu D1, Zhang C2, Sun H1, Shi W1, Kong F2, Feng X1.
Topical use of ginsenosides, the major bioactive substances in Panax ginseng, has been used for the treatment of irritated skin complaints. However, the protective mechanisms of ginsenosides remain unclear. In the present study, we investigated the anti-inflammatory role of ginsenoside F2 (GF2) on the skin inflammation. To induce irritant dermatitis, 12-O-tetradecanoylphorbol-13-acetate (TPA) was applied on the surface of the mouse ears with or without treatments of GF2 and dexamethasone for 24 h. Protective effects of GF2 on edema and inflammation were assessed by measuring ear thickness, weights of skin punch, and inflammatory responses. In gross findings, treatments with GF2 significantly decreased skin thickness and weight compared to those of TPA-treated groups, which was comparable with the protective effects of dexamethasone. In addition, expression of inflammatory mediators was remarkably reduced in GF2-treated ears compared to that of vehicle-treated ears of mice. Interestingly, immunohistochemistry and flow cytometry analyses revealed that TPA treatment significantly increased infiltration of interleukin-17 (IL-17) producing dermal γδ T cells, while frequencies of γδ T cells was decreased by GF2 treatment, subsequently ameliorating inflammation in skin. Concomitantly, TPA-mediated skin inflammation was significantly ameliorated in IL-17A knock out mice. Furthermore, GF2 treatment inhibited infiltration and generation of reactive oxygen species (ROS) of neutrophils in damaged ears compared with vehicle-treated mice. These results clearly suggest that GF2 treatment ameliorates TPA-induced dermal inflammation by inhibiting production of IL-17 and ROS in γδ T cells and neutrophils, respectively. Therefore, as a natural compound, application of GF2 may be a novel therapeutic approach for treating skin inflammation.
Copyright © 2016 Elsevier Inc. All rights reserved.
Interleukin-17; Neutrophil; ROS; γδ T cell
Protective effects of ginsenoside F2 on 12-O-tetradecanoylphorbol-13-acetate-induced skin inflammation in mice.
Park SH1, Seo W2, Eun HS3, Kim SY4, Jo E4, Kim MH4, Choi WM4, Lee JH4, Shim YR4, Cui CH5, Kim SC6, Hwang CY1, Jeong WI7.
2016 Sep 30
Ginsenoside F2, a metabolite from Ginsenoside Rb1, induces apoptosis accompanied by protective autophagy in breast cancer stem cells.