Premium
Astaxanthin, a xanthophyll carotenoid, inhibits ultraviolet‐induced apoptosis in keratinocytes
Author(s) -
Yoshihisa Yoko,
Rehman Mati ur,
Shimizu Tadamichi
Publication year - 2014
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12347
Subject(s) - hacat , astaxanthin , apoptosis , reactive oxygen species , chemistry , nitric oxide , dna fragmentation , xanthophyll , microbiology and biotechnology , zeaxanthin , carotenoid , biochemistry , biology , programmed cell death , lutein , in vitro , organic chemistry
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 μ m ) caused a significant decrease in the protein content and the m RNA levels of inducible nitric oxide (i NOS ) 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 m RNA expression of macrophage migration inhibitory factor (MIF), IL‐1 β and TNF‐ α in HaCaT keratinocytes. These results suggest that AST effectively protects against UV‐induced inflammation by decreasing i NOS and COX‐2, and thereby inhibiting the apoptosis of keratinocytes.