Ginsenoside F1

Role of epidermal γδ T-cell-derived interleukin 13 in the skin-whitening effect of Ginsenoside F1.[Pubmed: 25091975]

Exp Dermatol. 2014 Nov;23(11):860-2.

Ginsenoside F1 (GF1) is a metabolite of ginsenoside Rg1. Although Ginsenoside F1 has several benefits for skin physiology, the effect of Ginsenoside F1 on skin pigmentation has not been reported.
METHODS AND RESULTS:
We found that a cream containing 0.1% Ginsenoside F1 showed a significant whitening effect on artificially tanned human skin after 8 weeks of application. However, Ginsenoside F1 did not inhibit mRNA expression of tyrosinase or dopachrome tautomerase (DCT) in normal human epidermal melanocytes (NHEMs) or cocultured NHEMs/normal human epidermal keratinocytes. Interestingly, Ginsenoside F1 enhanced production of interleukin 13 (IL-13) from human epidermal γδ T cells. IL-13 significantly reduced the mRNA expression and protein amount of both tyrosinase and DCT and reduced melanin synthesis activities in NHEMs, resulting in visible brightening of NHEM pellet.
CONCLUSIONS:
These results suggest that enhancement of IL-13 production by Ginsenoside F1 from epidermal γδ T cells might play a role in the skin-whitening effect of GF1 via the suppression of tyrosinase and DCT.

Ginsenoside F1 Modulates Cellular Responses of Skin Melanoma Cells.[Reference: WebLink]

J. Ginseng Res., 2011, 35(1):86-91.

Ginsenoside F1 (G-F1) is an enzymatic metabolite generated from G-Rg1. Although this metabolite has been reported to suppress platelet aggregation and to reduce gap junction-mediated intercellular communication, the modulatory activity of G-F1 on the functional role of skin-derived cells has not yet been elucidated.
METHODS AND RESULTS:
In this study, we evaluated the regulatory role of G-F1 on the cellular responses of B16 melanoma cells. G-F1 strongly suppressed the proliferation of B16 cells up to 60% at 200 ug/mL, while only diminishing the viability of HEK293 cells up to 30%. Furthermore, G-F1 remarkably induced morphological change and clustering of B16 melanoma cells. The melanin production of B16 cells was also significantly blocked by G-F1 up to 70%. Interestingly, intracellular signaling events involved in cell proliferation, migration, and morphological change were up-regulated at 1 h incubation but down-regulated at 12 h.
CONCLUSIONS:
Therefore, our results suggest that G-F1 can be applied as a novel anti-skin cancer drug with anti-proliferative and anti-migration features.

Inhibitory effect of elastase and tyrosinase of ginsenoside F1 isolated from Panax ginseng leaves[Reference: WebLink]

Korean Journal of Pharmacognosy, 2013, 44(1):10-15.

This study was carried to establish a simple isolation and purification method of Ginsenoside F1 from leaves of Panax ginseng and was to evaluate the inhibitory effect of purified Ginsenoside F1 on the activities of elastase and tyrosinase.
METHODS AND RESULTS:
The content of Ginsenoside F1 was 90-fold higher in leaves than in root of ginseng. Ginsenoside F1 was isolated from EtOAc fraction between EtOAc and alkalized water of 80% EtOH extract after remove of hydrophobic components. The 50% inhibitory concentration (IC50) of Ginsenoside F1 on elastase activity and tyrosinase activity was 1.07 mM and 1.81 mM, respectively. Especially, inhibitory effect of Ginsenoside F1 on tyrosinase activity was higher than that of arbutin (IC50; 2.20 mM).
CONCLUSIONS:
These results indicate that Ginsenoside F1 have a potential for industrial cosmetic materials.

Ginsenoside F1 protects human HaCaT keratinocytes from ultraviolet-B-induced apoptosis by maintaining constant levels of Bcl-2.[Pubmed: 12925222]

Ginsenoside F1 attenuates hyperpigmentation in B16F10 melanoma cells by inducing dendrite retraction and activating Rho signalling.[Pubmed: 25381719]

Exp Dermatol. 2015 Feb;24(2):150-2.

Ginsenoside F1 (GF1) is a metabolite produced by hydrolysis of the ginsenoside Re and Rg1 in Panax ginseng. According to various studies, high amounts of ginseng components are absorbed in the metabolized form, which are key constituents responsible for the biological effects of P. ginseng. Recently, GF1 was reported to have beneficial effects on skin. However, there has not been a sound understanding of its antimelanogenic effect and underlying molecular mechanisms.
METHODS AND RESULTS:
In this study, GF1 reduced α-melanocyte-stimulating hormone-induced melanin secretion in B16F10 cell culture media by 60%. However, it did not suppress intracellular melanin levels, tyrosinase activity and expression. Immunofluorescence assay showed that GF1 had no effect on melanosome transport, but significantly induced dendrite retraction. Pull-down assay demonstrated that GF1 primarily modulates the Rho family GTPases resulting in dendrite retraction.
CONCLUSIONS:
Collectively, these data suggest that GF1 could act as a potent skin-whitening agent.

J Invest Dermatol. 2003 Sep;121(3):607-13.

Ginsenosides, the major active ingredients of ginseng, show a variety of biomedical efficacies such as antiaging and antioxidation. Here, we investigate the protective activity of the Ginsenoside F1, an enzymatically modified derivative of ginsenoside Rg1, against ultraviolet-B-induced damage in human HaCaT keratinocytes.
METHODS AND RESULTS:
Ginsenoside F1 significantly reduced ultraviolet-B-induced cell death and protected HaCaT cells from apoptosis caused by ultraviolet B irradiation. Furthermore, Ginsenoside F1 prevented ultraviolet-B-induced cleavage of poly(ADP-ribose) polymerase in HaCaT cells.
CONCLUSIONS:
In search of the molecular mechanism responsible for the antiapoptotic effect of Ginsenoside F1, we find that protection from ultraviolet-B-induced apoptosis is tightly correlated with ginsenoside-F1-mediated inhibition of ultraviolet-B-induced downregulation of Bcl-2 and Brn-3a expression.