Gomisin N Inhibits Melanogenesis through Regulating the PI3K/Akt and MAPK/ERK Signaling Pathways in Melanocytes
- Authors
- Chae, Jae Kyoung; Subedi, Lalita; Jeong, Minsun; Park, Yong Un; Kim, Chul Young; Kim, Hakwon; Kim, Sun Yeou
- Issue Date
- Feb-2017
- Publisher
- MDPI
- Keywords
- Schisandra chinensis; Gomisin N; lignan; melanogenesis; skin whitening
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.18, no.2
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Volume
- 18
- Number
- 2
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6458
- DOI
- 10.3390/ijms18020471
- ISSN
- 1422-0067
- Abstract
- Gomisin N, one of the lignan compounds found in Schisandra chinensis has been shown to possess anti-oxidative, anti-tumorigenic, and anti-inflammatory activities in various studies. Here we report, for the first time, the anti-melenogenic efficacy of Gomisin N in mammalian cells as well as in zebrafish embryos. Gomisin N significantly reduced the melanin content without cellular toxicity. Although it was not capable of modulating the catalytic activity of mushroom tyrosinase in vitro, Gomisin N downregulated the expression levels of key proteins that function in melanogenesis. Gomisin N downregulated melanocortin 1 receptor (MC1R), adenylyl cyclase 2, microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein-1 (TRP-1), and tyrosinase-related protein-2 (TRP-2). In addition, Gomisin N-treated Melan-A cells exhibited increased p-Akt and p-ERK levels, which implies that the activation of the PI3K/Akt and MAPK/ERK pathways may function to inhibit melanogenesis. We also validated that Gomisin N reduced melanin production by repressing the expression of MITF, tyrosinase, TRP-1, and TRP-2 in mouse and human cells as well as in developing zebrafish embryos. Collectively, we conclude that Gomisin N inhibits melanin synthesis by repressing the expression of MITF and melanogenic enzymes, probably through modulating the PI3K/Akt and MAPK/ERK pathways.
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