The effect of emodin on melanogenesis through the modulation of ERK and MITF signaling pathway

Nat Prod Res. 2022 Feb;36(4):1084-1088. doi: 10.1080/14786419.2020.1849200. Epub 2020 Nov 18.

Abstract

The aim of this study was to investigate the effect of emodin derived from Polygonum multiflorum on melanin production in B16F1 cells. In this study, emodin did not show antioxidant activity in DPPH radical and reducing power assays. However, it was found that emodin scavenged intracellular H2O2. Emodin increased not only tyrosinase activity but also melanin synthesis in vitro. Moreover, emodin enhanced melanin synthesis by increasing the expression level of tyrosinase (TYR), tyrosine related protein (TRP)-1, TRP-2, MITF and SIRT1 proteins in live cells treated with H2O2 compared with H2O2 treatment group in the analyses of western blot and immunofluorescence. Moreover, emodin suppressed ERK activation by SIRT1 and FOXO1. Thus, emodin promoted melanin synthesis by increasing the expression of TRP-1, TRP-2, tyrosinase through the activation of MITF transcription factor. These findings suggest that emodin could promote melanin production related to anti-hair graying.

Keywords: ERK; Emodin; MITF; SIRT1; melanogenesis.

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Emodin* / pharmacology
  • Extracellular Signal-Regulated MAP Kinases
  • Fallopia multiflora / chemistry*
  • Hydrogen Peroxide / pharmacology
  • Melanins / biosynthesis*
  • Melanoma, Experimental
  • Microphthalmia-Associated Transcription Factor
  • Monophenol Monooxygenase / metabolism
  • Signal Transduction / drug effects*

Substances

  • Melanins
  • Microphthalmia-Associated Transcription Factor
  • Hydrogen Peroxide
  • Monophenol Monooxygenase
  • Extracellular Signal-Regulated MAP Kinases
  • Emodin