Background: Ginsenosides of are used to enhance skin health and beauty. The present study aimed to investigate the potential use of ginsenoside Rf (Rf) from as a new anti-pigmentation agent.
Methods: The anti-melanogenic effects of Rf were explored. The transcriptional activity of the cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) and the expression levels of tyrosinase, microphthalmia-associated transcription factor (MITF), and tyrosinase-related proteins (Tyrps) were evaluated in melanocytes and UV-irradiated human skin.
Results: Rf significantly inhibited Forskolin (FSK) or UV-stimulated melanogenesis. Consistently, cellular tyrosinase activity and levels of MITF, tyrosinase, and Tyrps were downregulated. Furthermore, Rf suppressed MITF promoter activity, which was stimulated by FSK or CREB-regulated transcription coactivator 3 (CRTC3) overexpression. Increased CREB phosphorylation and protein kinase A (PKA) activity induced by FSK were also mitigated in the presence of Rf.
Conclusion: Rf can be used as a reliable anti-pigmentation agent, which has a scientifically confirmed and reproducible action mechanism, via inhibition of CREB/MITF pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8587488 | PMC |
| http://dx.doi.org/10.1016/j.jgr.2020.11.003 | DOI Listing |
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Article Synopsis
- MC1R is a receptor in melanocytes that regulates melanin production via α-MSH, while TLR4, found in various cell types, activates immune responses and also enhances melanin production through the NF-κB pathway.
- Benzimidazole-2-butanol (BI2B) has been identified as an inhibitor of the LPS/TLR4 pathway and shows potential in reducing excess pigmentation by targeting the α-MSH-induced melanogenic process.
- In tests involving UV-B-irradiated mouse skin and activated melanocyte cultures, BI2B effectively decreased levels of melanogenic markers and disrupted key signaling pathways linked to pigmentation, highlighting its role in managing hyperpigmentation.
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