Ip Is Decreased Melanogenesis Using Inhibition of PKA

Melanogenesis is essential UV protection mechanism in skin. However, excessive melanogenesis causes hyperpigmentation deceases, such as a melasma, freckle, etc. Therefore, through depigmentation agents, it is necessary to regulate melanogenesis. In this study, we identified noble whitening agent and their molecular mechanism. Firstly, we show that IP led to decrease melanin contents in a dose dependent manner in B16F10. The decrease of melanin synthesis was occurred by IP mediated decreasing Tyrosinase activity and expression. In general, Tyroainase expression is regulated by Microphthalmia-associated transcription factor (MITF) in a-MSH treated B16F10. Thus, we identified change of MITF activity in IP treated B16F10. IP down-regulated MITF activity and also MITF expression in a-MSH treated B16F10. Next, we identified CREB activity and phosphorylation in IP-treated B16F10, because CREB activity is implicated in MITF expression in a-MSH mediated melanogenesis. As shown our result, IP decreased CREB activity and phosphorylation in B16F10. Additionally, as CREB is phosphorylated by PKA, we showed PKA activity using phosphor-PKA. Phosphor-PKA was up-regulated by IP in B16F10. Overall, IP regulates melanin synthesis using regulation of PKA-CREB-MITF-Tyrosinase axis.

Acknowledgments

This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2017R1D1A1B03028380).