Extract of Deschampsia antarctica (EDA) Prevents Dermal Cell Damage Induced by UV Radiation and 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Int J Mol Sci. 2019 Mar 18;20(6):1356. doi: 10.3390/ijms20061356.

Abstract

Exposure to natural and artificial light and environmental pollutants are the main factors that challenge skin homeostasis, promoting aging or even different forms of skin cancer through a variety of mechanisms that include accumulation of reactive oxygen species (ROS), engagement of DNA damage responses, and extracellular matrix (ECM) remodeling upon release of metalloproteases (MMPs). Ultraviolet A radiation is the predominant component of sunlight causative of photoaging, while ultraviolet B light is considered a potentiator of photoaging. In addition, different chemicals contribute to skin aging upon penetration through skin barrier disruption or hair follicles, aryl hydrocarbon receptors (AhR) being a major effector mechanism through which toxicity is exerted. Deschampsia antarctica is a polyextremophile Gramineae capable of thriving under extreme environmental conditions. Its aqueous extract (EDA) exhibits anti- photoaging in human skin cells, such as inhibition of MMPs, directly associated with extrinsic aging. EDA prevents cellular damage, attenuating stress responses such as autophagy and reducing cellular death induced by UV. We demonstrate that EDA also protects from dioxin-induced nuclear translocation of AhR and increases the production of loricrin, a marker of homeostasis in differentiated keratinocytes. Thus, our observations suggest a potential use exploiting EDA's protective properties in skin health supplements.

Keywords: dermal fibroblast; dioxins; in vitro studies; keratinocytes; natural extract; photoaging; ultraviolet light.

MeSH terms

  • Caspase 3 / metabolism
  • Cell Nucleus / drug effects
  • Cell Nucleus / metabolism
  • Cell Nucleus / radiation effects
  • Cell Shape / drug effects
  • Cell Shape / radiation effects
  • DNA Damage
  • Dermis / pathology*
  • Dermis / radiation effects*
  • Fibroblasts / drug effects
  • Fibroblasts / pathology
  • Fibroblasts / radiation effects
  • Histones / metabolism
  • Humans
  • Keratinocytes / drug effects
  • Keratinocytes / pathology
  • Keratinocytes / radiation effects
  • Matrix Metalloproteinase 1 / metabolism
  • Membrane Proteins / metabolism
  • Microtubule-Associated Proteins / metabolism
  • Plant Extracts / pharmacology*
  • Poaceae / chemistry*
  • Poly(ADP-ribose) Polymerases / metabolism
  • Polychlorinated Dibenzodioxins / toxicity*
  • Receptors, Aryl Hydrocarbon / metabolism
  • Signal Transduction
  • Stress, Physiological / drug effects
  • Stress, Physiological / radiation effects
  • Ultraviolet Rays*

Substances

  • H2AX protein, human
  • Histones
  • MAP1LC3A protein, human
  • Membrane Proteins
  • Microtubule-Associated Proteins
  • Plant Extracts
  • Polychlorinated Dibenzodioxins
  • Receptors, Aryl Hydrocarbon
  • loricrin
  • Poly(ADP-ribose) Polymerases
  • Caspase 3
  • Matrix Metalloproteinase 1