title: Astaxanthin, a xanthophyll carotenoid, inhibits ultraviolet-induced apoptosis in keratinocytes.
abstract: 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.
authors: Department of Dermatology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan.
authors: Yoko
authors: Y
authors: Yoshihisa
authors: Mati Ur
authors: MU
authors: Rehman
authors: Tadamichi
authors: T
authors: Shimizu
mesh_terms: D017209:Apoptosis / Q000187:drug effects* / Q000528:radiation effects; D053453:Caspase 9 / Q000378:metabolism; D002460:Cell Line; D002470:Cell Survival; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D006801:Humans; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects* / Q000378:metabolism* / Q000528:radiation effects; D008263:Macrophage Migration-Inhibitory Factors / Q000235:genetics / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D014466:Ultraviolet Rays; D024341:Xanthophylls / Q000494:pharmacology; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494826:BAX protein, human; D053583:Interleukin-1beta; D008263:Macrophage Migration-Inhibitory Factors; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D024341:Xanthophylls; D051028:bcl-2-Associated X Protein; C005948:astaxanthine; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D011065:Poly(ADP-ribose) Polymerases; D053453:Caspase 9; D015232:Dinoprostone
keywords: apoptosis; astaxanthin; keratinocyte; reactive oxygen species; ultraviolet