Astaxanthin, a xanthophyll carotenoid, inhibits ultraviolet-induced apoptosis in keratinocytes

Exp Dermatol. 2014 Mar;23(3):178-83. doi: 10.1111/exd.12347.


Intra-cellular reactive nitrogen/oxygen species and apoptosis play important roles in ultraviolet (UV)-induced inflammatory responses in the skin. Astaxanthin (AST), a xanthophyll carotenoid, exhibits diverse clinical benefits. The protective effects of AST against UV-induced apoptosis were investigated in the present study. Astaxanthin (5 μm) caused a significant decrease in the protein content and the mRNA levels of inducible nitric oxide (iNOS) and cyclooxygenase (COX)-2, and decreased the release of prostaglandin E2 from HaCaT keratinocytes after UVB (20 mJ/cm(2) ) or UVC (5 mJ/cm(2) ) irradiation. No significant protective effects against UV-induced reactive oxygen species (ROS) were observed in AST-pretreated cells. Astaxanthin caused a significant inhibition of UV-irradiation-induced apoptosis, as evidence by a DNA fragmentation assay. Furthermore, we found that the treatment with AST caused a reduction in the UVB- or UVC-induced protein and mRNA expression of macrophage migration inhibitory factor (MIF), IL-1β and TNF-α in HaCaT keratinocytes. These results suggest that AST effectively protects against UV-induced inflammation by decreasing iNOS and COX-2, and thereby inhibiting the apoptosis of keratinocytes.

Keywords: apoptosis; astaxanthin; keratinocyte; reactive oxygen species; ultraviolet.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / radiation effects
  • Caspase 9 / metabolism
  • Cell Line
  • Cell Survival
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism
  • Dinoprostone / metabolism
  • Humans
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Keratinocytes / drug effects*
  • Keratinocytes / metabolism*
  • Keratinocytes / radiation effects
  • Macrophage Migration-Inhibitory Factors / genetics
  • Macrophage Migration-Inhibitory Factors / metabolism
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Poly(ADP-ribose) Polymerases / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • RNA, Messenger / metabolism
  • Reactive Oxygen Species / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism
  • Ultraviolet Rays
  • Xanthophylls / pharmacology
  • bcl-2-Associated X Protein / metabolism


  • BAX protein, human
  • Interleukin-1beta
  • Macrophage Migration-Inhibitory Factors
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • Xanthophylls
  • bcl-2-Associated X Protein
  • astaxanthine
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • Poly(ADP-ribose) Polymerases
  • Caspase 9
  • Dinoprostone