6-Shogaol Protects Human Melanocytes against Oxidative Stress through Activation of the Nrf2-Antioxidant Response Element Signaling Pathway

Int J Mol Sci. 2020 May 16;21(10):3537. doi: 10.3390/ijms21103537.

Abstract

Skin is a major target of oxidative stress. Increasing evidence suggests that oxidative stress is the cause of melanocyte disappearance in vitiligo, which is an acquired pigmentary skin disorder characterized by patches of skin that have lost pigmentation. New herbal extracts with antioxidant activity are therefore being studied. 6-Shogaol (6-SG), an active compound from ginger, is capable of attenuating oxidative stress-induced ageing and neurotoxicity. Subsequently, to investigate whether 6-SG could protect melanocytes from oxidative stress, cultured human primary epidermal melanocytes (HEMn-MPs) were treated with hydrogen peroxide (H2O2) in the presence or absence of 6-SG. The 6-SG exhibited protective effects against H2O2-induced cell death by reducing oxidative stress. In addition, the 6-SG treatment activated the Nrf2-antioxidant response element signaling pathway by upregulating the mRNA expression of the antioxidant enzyme heme oxygenase 1 (HO-1), and protein expression of Nrf2, NAD(P)H: quinine oxidoreductase 1 (Nqo1), and HO-1. Furthermore, the 6-SG also displayed protective effects on melanocytes against Rhododendrol-induced oxidative stress. We concluded that 6-SG protects melanocytes against oxidative stress in vitro, and its protective effect is associated with the activation of the Nrf2-antioxidant response element signaling pathway. 6-SG, therefore, has potential for use in the prevention of melanocyte loss in the early stages of vitiligo or other pigmentary disorders.

Keywords: melanocyte; oxidative stress; shogaol.

MeSH terms

  • Antioxidant Response Elements / genetics*
  • Butanols
  • Catechols / pharmacology*
  • Cell Death / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Cytoprotection* / drug effects
  • Epidermis / pathology
  • Gene Expression Regulation / drug effects
  • Humans
  • Hydrogen Peroxide / toxicity
  • Infant, Newborn
  • Melanins / biosynthesis
  • Melanocytes / drug effects
  • Melanocytes / metabolism*
  • Melanocytes / pathology*
  • NF-E2-Related Factor 2 / metabolism*
  • Oxidative Stress* / drug effects
  • Oxidative Stress* / genetics
  • Signal Transduction*

Substances

  • Butanols
  • Catechols
  • Melanins
  • NF-E2-Related Factor 2
  • rhododendrol
  • shogaol
  • Hydrogen Peroxide