The Anti-Vitiligo Effects of Feshurin In Vitro from and the Mechanism of Action
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Background: Vitiligo is a complex disorder characterized by skin depigmentation; the canonical Wnt signaling pathway that involves -catenin plays a crucial role in promoting the melanin production in melanocytes. Targeted inhibition of the Janus kinase JAK-STAT pathway can effectively diminish the secretion of the chemokine C-X-C motif ligand CXCL10, thereby safeguarding melanocytes. has been applied as a treatment regimen for a long period; however, its use for the treatment of vitiligo has not been previously documented.
Methods: CCK-8 assay, Intracellular melanin content assay, Tyrosinase activity assay, Western blotting, qRT-PCR, and ELISA methods were employed. Using molecular docking verified the inhibitory effects of feshurin on the JAK1.
Results: The sesquiterpene coumarin feshurin was separated from . Feshurin was shown to induce GSK-3 phosphorylation, resulting in the translocation of -catenin into the nucleus. This translocation subsequently upregulated the transcription of microphthalmia-associated transcription factor (MITF), leading to increased tyrosinase activity and melanin production. In addition, feshurin inhibited the production of chemokine CXCL10 via the JAK-STAT signaling pathway, which was verified by molecular docking.
Conclusions: Based on these findings, it can be concluded that feshurin exhibits significant potential for the development of novel anti-vitiligo therapeutics.
Lee Y, Hyun C Int J Mol Sci. 2024; 25(22).
PMID: 39596485 PMC: 11594713. DOI: 10.3390/ijms252212421.