Inhibition of melanogenesis by sodium 2-mercaptoethanesulfonate
Jeong-Hwan Kim1,2,3,#, Chang-Taek Oh2,#, Tae-Rin Kwon2, Jong Hwan Kim2,3, Dong-Ho Bak2,3, Hyuk Kim1, Won-Seok Park1, and Beom Joon Kim2,3,*
1R&D Unit, AmorePacific Corporation, Yongin 17074, 2Department of Dermatology, Chung-Ang University College of Medicine, 3Department of Medicine, Graduate School, Chung-Ang University, Seoul 06974, Korea
Received: July 26, 2019; Revised: December 3, 2019; Accepted: January 14, 2020
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Sodium 2-mercaptoethanesulfonate (mesna) is a protective agent that is widely used in medicine because of its antioxidant effects. Recently, reactive oxygen species (ROS) were shown to increase pigmentation. Thus, ROS scavengers and inhibitors of ROS production may suppress melanogenesis. Forkhead box-O3a (FoxO3a) is an antimelanogenic factor that mediates ROS-induced skin pigmentation. In this study, we aimed to investigate the whitening effect of mesna and the signaling mechanism mediating this effect. Human melanoma (MNT-1) cells were used in this study. mRNA and protein expression were measured by real-time quantitative PCR and Western blotting analysis to track changes in FoxO3a-related signals induced by mesna. An immunofluorescence assay was performed to determine the nuclear translocation of FoxO3a. When MNT-1 melanoma cells were treated with mesna, melanin production and secretion decreased. These effects were accompanied by increases in FoxO3a activation and nuclear translocation, resulting in downregulation of four master genes of melanogenesis: MITF, TYR, TRP1, and TRP2. We found that mesna, an antioxidant and radical scavenger, suppresses melanin production and may therefore be a useful agent for the clinical treatment of hyperpigmentation disorders.