Daphne odora Exerts Depigmenting Effects via Inhibiting CREB/MITF and Activating AKT/ERK-Signaling Pathwaysopen access
- Authors
- Eom, Young Sic; Jeong, Dongho; Ryu, A-Reum; Song, Keon-Hyoung; Im, Dai Sig; Lee, Mi-Young
- Issue Date
- Aug-2022
- Publisher
- Caister Academic Press
- Keywords
- Daphne adora; depigmenting agent; anti-melanogenesis; CREB; MITF; AKT; ERK
- Citation
- Current Issues in Molecular Biology, v.44, no.8, pp 3312 - 3323
- Pages
- 12
- Journal Title
- Current Issues in Molecular Biology
- Volume
- 44
- Number
- 8
- Start Page
- 3312
- End Page
- 3323
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/21276
- DOI
- 10.3390/cimb44080228
- ISSN
- 1467-3037
1467-3045
- Abstract
- Daphne odora, a blooming shrub, has been traditionally used for various medicinal purposes. However, information on its anti-melanogenic activity and dermal application is limited. In this study, the Daphne odora extract (DOE), with constituents including daphnetin, was used to investigate depigmenting activity and the underlying mechanism of Daphne odora. DOE inhibited in vitro and cellular tyrosinase activity in a dose-dependent manner, and reduced the alpha-MSH-induced melanin biosynthesis to a control level. The protein expressions of melanin synthesis-related enzymes were also significantly reduced by DOE. Moreover, DOE decreased the phosphorylation of cAMP-response element binding proteins (CREBs) induced by alpha-MSH in B16F10 cells, while it activated phosphorylated extra-cellular signal-regulated kinases (ERKs) and protein kinase B (AKT) expression. These results suggest that DOE might inhibit the melanogenesis signaling pathways by activating ERK- and AKT-signaling pathways to regulate the expression of CREB and MITF and its downstream pathways. Therefore, DOE could potentially be developed as a depigmenting agent.
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- Appears in
Collections - College of Medical Sciences > Department of Medical Biotechnology > 1. Journal Articles
- College of Medical Sciences > Department of Pharmaceutical Engineering > 1. Journal Articles
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