Metformin inhibits the inflammatory and oxidative stress response induced by skin UVB-irradiation and provides 4-hydroxy-2-nonenal and nitrotyrosine formation and p53 protein activation

J Dermatol Sci. 2020 Nov;100(2):152-155. doi: 10.1016/j.jdermsci.2020.05.012. Epub 2020 Jun 2.
No abstract available

Keywords: Metformin; Oxidative stress; Skin immune response; UVB skin damage.

Publication types

  • Letter

MeSH terms

  • Aldehydes / metabolism
  • Animals
  • Carcinogenesis / drug effects
  • Carcinogenesis / immunology
  • Carcinogenesis / radiation effects
  • DNA Damage / immunology
  • DNA Damage / radiation effects
  • Female
  • Humans
  • Melanoma / etiology
  • Melanoma / pathology
  • Melanoma / prevention & control
  • Metformin / pharmacology*
  • Metformin / therapeutic use
  • Mice
  • Oxidative Stress / drug effects*
  • Oxidative Stress / genetics
  • Oxidative Stress / immunology
  • Radiation Injuries, Experimental / immunology
  • Radiation Injuries, Experimental / pathology
  • Radiation Injuries, Experimental / prevention & control*
  • Radiodermatitis / immunology
  • Radiodermatitis / pathology
  • Radiodermatitis / prevention & control*
  • Skin / drug effects
  • Skin / immunology
  • Skin / pathology
  • Skin / radiation effects
  • Skin Neoplasms / etiology
  • Skin Neoplasms / pathology
  • Skin Neoplasms / prevention & control
  • Tumor Suppressor Protein p53 / metabolism*
  • Tyrosine / analogs & derivatives
  • Tyrosine / metabolism
  • Ultraviolet Rays / adverse effects

Substances

  • Aldehydes
  • Trp53 protein, mouse
  • Tumor Suppressor Protein p53
  • 3-nitrotyrosine
  • Tyrosine
  • Metformin
  • 4-hydroxy-2-nonenal