Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signalingopen access
- Moon, Sun Young; Akter, Kazi-Marjahan; Ahn, Mi-Jeong; Kim, Kwang Dong; Yoo, Jiyun; Lee, Joon-Hee; Lee, Jeong-Hyung; Hwangbo, Cheol
- Issue Date
- fraxinol; B16-F10 cells; melanogenesis; microphthalmia-associated transcription factor; depigmentation
- MOLECULES, v.27, no.5
- Journal Title
- 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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- 농업생명과학대학 > 동물생명융합학부 > Journal Articles
- 약학대학 > 약학과 > Journal Articles
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