Biological and Pharmaceutical Bulletin
Online ISSN : 1347-5215
Print ISSN : 0918-6158
ISSN-L : 0918-6158

この記事には本公開記事があります。本公開記事を参照してください。
引用する場合も本公開記事を引用してください。

Scopoletin stimulates melanogenesis via cAMP/PKA pathway and partially p38 activation
Dae-Sung KimSu-Bin ChaMin-Cheol ParkSeol-A ParkHye-Soo KimWon-Hong WooYeun-Ja Mun
著者情報
ジャーナル フリー 早期公開

論文ID: b16-00690

この記事には本公開記事があります。
詳細
抄録

Scopoletin was recently shown to stimulate melanogenesis through cAMP-response element-binding protein (CREB) phosphorylation. In this study, we investigated the molecular events of melanogenesis-induced by scopoletin. After exposure to scopoletin, the protein levels of tyrosinase and tyrosianse related protein-1 (TRP-1) were significantly increased in B16F10 cells. The mRNA levels of tyrosinase and microphthalmia-associated transcription factor (MITF) were also enhanced by scopoletin. cAMP production and phosphorylation of p38 mitogen-activated protein kinase (MAPK) were increased by scopoletin treatment. Scopoletin-mediated increase of intracellular melanin and tyrosinase expression were significantly attenuated by PKA inhibitors (H-89 and KT5720), while a PKC inhibitor (Ro-32-0432) had no effect and a p38 MAPK inhibitor (SB203580) partially blocked the scopoletin-induced intracellular melanin and tyrosinase expression. Moreover, scopoletin synergistically with cell-permeable cAMP analog (dibutyryl cAMP) significantly induced tyrosinase activity and melanin content in B16F10 cells. The silencing of p38 MAPK by siRNA decreased the scopoletin-induced tyrosinase expression in B16F10 cells. These results suggest that scopoletin could induce melanin synthesis through the cAMP/PKA pathway and partially p38 MAPK activation in B16F10 cells.

著者関連情報
© 2017 The Pharmaceutical Society of Japan
feedback
Top