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Angelica dahurica attenuates melanogenesis in B16F0 cells by repressing Wnt/β-catenin signaling

Background Melanogenesis is a complex process which is tightly regulated by several enzymes. However, abnormal melanogenesis can cause severe dermatological problems. Roots of Angelica dahurica have been used for skin care as a part of traditional Chinese medicine for many generations. However, the...

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Published in:Molecular & cellular toxicology 2023, 19(1), , pp.135-143
Main Authors: Fang, Chien-Liang, Goswami, Debakshee, Kuo, Chia-Hua, Day, Cecilia Hsuan, Lin, Mei-Yi, Ho, Tsung-Jung, Yang, Liang-Yo, Hsieh, Dennis Jine-Yuan, Lin, Tzu-Kai, Huang, Chih-Yang
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Language:English
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Summary:Background Melanogenesis is a complex process which is tightly regulated by several enzymes. However, abnormal melanogenesis can cause severe dermatological problems. Roots of Angelica dahurica have been used for skin care as a part of traditional Chinese medicine for many generations. However, the role of A. dahurica in melanogenesis remains unclear. Objective Previous in vitro and in vivo studies have demonstrated that NK-1R exerts positive effects in melanogenesis via the Wnt/βcatenin signaling pathway. In this study, we investigated the effects of A. dahurica ethanol extract (ADE) on NK-1R and Wnt/β-catenin signaling, and evaluated the effect of NK-1R on melanogenesis in B16F0 cells. Results Angelica dahurica ethanol extract efficiently downregulated Neurokinin-1 receptor and Wnt/β-catenin signaling by decreasing the expression of β-catenin, MITF, LEF-1, TYR, TRP1, and TRP2 and increasing the expression of GSK3β, which resulted from the weakened expression of the Neurokinin-1 receptor inhibitor [Sar9,Met(O 2 )11 ]-Substance P (SMSP). Furthermore, the intracellular melanin assay and cellular tyrosinase activity confirmed these findings. Conclusion This study suggests that ADE has potential to downregulate Neurokinin-1 receptor in SMSP-induced B16F0 cells, thereby repressing the Wnt/β-catenin signaling and reduces melanin production. Graphical abstract
ISSN:1738-642X
2092-8467
DOI:10.1007/s13273-022-00250-0