Hydroxytyrosol from olive fruits prevents blue-light-induced damage in human keratinocytes and fibroblasts

J Cell Physiol. 2019 Jun;234(6):9065-9076. doi: 10.1002/jcp.27584. Epub 2018 Oct 26.

Abstract

Skin aging is a complex biological process influenced by a combination of endogenous or intrinsic and exogenous or extrinsic factors due to environmental damage. The primary environmental factor that causes human skin aging is the ultraviolet irradiation from the sun. Recently, it was established that the long-term exposure to light-emitting-diode-generated blue light (LED-BL) from electronic devices seems to have a relevant implication in the molecular mechanisms of premature photoaging. BL irradiation induces changes in the synthesis of various skin structures through DNA damage and overproduction of reactive oxygen species (ROS), matrix metalloproteinase-1 and -12, which are responsible for the loss of the main components of the extracellular matrix of skin like collagen type I and elastin. In the current study, using human keratinocytes and fibroblasts exposed to specific LED-BL radiation doses (45 and 15 J/cm 2 ), we produced an in vitro model of skin photoaging. We verified that, compared with untreated controls, the treatment with LED-BL irradiation results in the alteration of metalloprotease-1 (collagenase), metalloprotease-12 (elastase), 8-dihydroxy-2'-deoxyguanosine, proliferating cell nuclear antigen, and collagen type I. Moreover, we showed that the photoaging prevention is possible via the use of hydroxytyrosol extracted from olive fruits, well known for antioxidant properties. Our results demonstrated that hydroxytyrosol protects keratinocytes and fibroblasts from LED-BL-induced damage. Thus, hydroxytyrosol might be proposed as an encouraging candidate for the prevention of BL-induced premature photoaging.

Keywords: antioxidants; blue light; cell culture; oxidative stress; photoaging; skin.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antioxidants / isolation & purification
  • Antioxidants / pharmacology*
  • Cell Line
  • Cell Survival / drug effects
  • Cell Survival / radiation effects
  • Collagen Type I / genetics
  • Collagen Type I / metabolism
  • DNA Damage
  • Elastin / metabolism
  • Fibroblasts / drug effects*
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Fibroblasts / radiation effects
  • Fruit* / chemistry
  • Humans
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism
  • Keratinocytes / pathology
  • Keratinocytes / radiation effects
  • Light / adverse effects*
  • Matrix Metalloproteinase 1 / genetics
  • Matrix Metalloproteinase 1 / metabolism
  • Matrix Metalloproteinase 12 / genetics
  • Matrix Metalloproteinase 12 / metabolism
  • Olea* / chemistry
  • Oxidative Stress / drug effects
  • Oxidative Stress / radiation effects
  • Phenylethyl Alcohol / analogs & derivatives*
  • Phenylethyl Alcohol / isolation & purification
  • Phenylethyl Alcohol / pharmacology
  • Proliferating Cell Nuclear Antigen / metabolism
  • Radiation-Protective Agents / isolation & purification
  • Radiation-Protective Agents / pharmacology*
  • Reactive Oxygen Species / metabolism
  • Skin / drug effects*
  • Skin / metabolism
  • Skin / pathology
  • Skin / radiation effects
  • Skin Aging / drug effects*
  • Skin Aging / radiation effects
  • Time Factors

Substances

  • Antioxidants
  • Collagen Type I
  • PCNA protein, human
  • Proliferating Cell Nuclear Antigen
  • Radiation-Protective Agents
  • Reactive Oxygen Species
  • 3,4-dihydroxyphenylethanol
  • Elastin
  • MMP12 protein, human
  • Matrix Metalloproteinase 12
  • MMP1 protein, human
  • Matrix Metalloproteinase 1
  • Phenylethyl Alcohol