Redox regulation of cellular stress response by ferulic acid ethyl ester in human dermal fibroblasts: role of vitagenes.
Clin Dermatol
; 26(4): 358-63, 2008.
Article
em En
| MEDLINE
| ID: mdl-18691515
ABSTRACT
Skin is one of the main targets for reactive oxygen species; thus, reactive oxygen species-induced damage and protein and lipid modifications occur, and skin can undergo a wide array of diseases, from photosensitivity to cancer. In this study, human dermal fibroblasts exposed to hydrogen peroxide (0-1000 micromol/L) exhibited a marked increase in both protein carbonyls and 4-hydroxy-2-nonenal, which are indices of protein and lipid oxidation, respectively. An amount of 25 micromol/L ferulic acid ethyl ester, a well-known nutritional antioxidant, significantly counteracted both protein and lipid oxidation and reduced the loss in cell viability elicited by 500 micromol/L of hydrogen peroxide. A common way for cells to react to oxidative stress is up-regulation of vitagenes. To the vitagene family belong the heat shock proteins heme oxygenase-1 and heat shock protein-70, which are involved in the cellular defense against oxidative stress by different mechanisms. The administration of 25 micromol/L ferulic acid ethyl ester significantly decreased hydrogen peroxide-induced protein and lipid oxidation. Dermal fibroblasts exposed to 25 micromol/L ferulic acid ethyl ester in the presence of 500 micromol/L hydrogen peroxide showed an increased level of both heme oxygenase-1 and heat shock protein-70 compared with dermal fibroblasts treated with hydrogen peroxide alone. These findings provide evidence for the protective role of vitagenes in free radical-induced skin damage and highlight the potential protective use of nutritional antioxidants, such as ferulic acid and its derivatives.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Pele
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Ácidos Cafeicos
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Estresse Oxidativo
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Proteínas de Choque Térmico HSP70
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Heme Oxigenase-1
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Fibroblastos
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Antioxidantes
Limite:
Humans
Idioma:
En
Ano de publicação:
2008
Tipo de documento:
Article