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Cited 8 time in webofscience Cited 8 time in scopus
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Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signalingopen access

Authors
Moon, Sun YoungAkter, Kazi-MarjahanAhn, Mi-JeongKim, Kwang DongYoo, JiyunLee, Joon-HeeLee, Jeong-HyungHwangbo, Cheol
Issue Date
Mar-2022
Publisher
MDPI
Keywords
fraxinol; B16-F10 cells; melanogenesis; microphthalmia-associated transcription factor; depigmentation
Citation
MOLECULES, v.27, no.5
Indexed
SCIE
SCOPUS
Journal Title
MOLECULES
Volume
27
Number
5
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/1562
DOI
10.3390/molecules27051549
ISSN
1420-3049
1420-3049
Abstract
Melanin pigment produced in melanocytes plays a protective role against ultraviolet radiation. Selective destruction of melanocytes causes chronic depigmentation conditions such as vitiligo, for which there are very few specific medical treatments. Here, we found that fraxinol, a natural coumarin from Fraxinus plants, effectively stimulated melanogenesis. Treatment of B16-F10 cells with fraxinol increased the melanin content and tyrosinase activity in a concentration-dependent manner without causing cytotoxicity. Additionally, fraxinol enhanced the mRNA expression of melanogenic enzymes such as tyrosinase, tyrosinase-related protein-1, and tyrosinase-related protein-2. Fraxinol also increased the expression of microphthalmia-associated transcription factor at both mRNA and protein levels. Fraxinol upregulated the phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB). Furthermore, H89, a cAMP-dependent protein kinase A inhibitor, decreased fraxinol-induced CREB phosphorylation and microphthalmia-associated transcription factor expression and significantly attenuated the fraxinol-induced melanin content and intracellular tyrosinase activity. These results suggest that fraxinol enhances melanogenesis via a protein kinase A-mediated mechanism, which may be useful for developing potent melanogenesis stimulators.
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