Dihydrocaffeic Acid Prevents UVB-Induced Oxidative Stress Leading to the Inhibition of Apoptosis and MMP-1 Expression via p38 Signaling Pathway

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  • Mariana M. Oliveira
    Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Maringá 87020-900, Brazil
  • Bianca A. Ratti
    Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Maringá 87020-900, Brazil
  • Regina G. Daré
    Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Maringá 87020-900, Brazil
  • Sueli O. Silva
    Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Maringá 87020-900, Brazil
  • Maria da Conceição T. Truiti
    Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Maringá 87020-900, Brazil
  • Tânia Ueda-Nakamura
    Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Maringá 87020-900, Brazil
  • Rachel Auzély-Velty
    Centre de Recherches sur les Macromolécules Végétales, Université Grenoble Alpes, Grenoble 38041, France
  • Celso V. Nakamura
    Programa de Pós-Graduação em Ciências Farmacêuticas, Universidade Estadual de Maringá, Maringá 87020-900, Brazil

書誌事項

公開日
2019-01-17
権利情報
  • http://creativecommons.org/licenses/by/4.0/
DOI
  • 10.1155/2019/2419096
公開者
Wiley

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説明

<jats:p>Chronic UVB exposure promotes oxidative stress, directly causes molecular damage, and induces aging-related signal transduction, leading to skin photoaging. Dihydrocaffeic acid (DHCA) is a phenolic compound with potential antioxidant capacity and is thus a promising compound for the prevention of UVB-induced skin photodamage. The aim of this study was to evaluate the antioxidant and protective effect of DHCA against oxidative stress, apoptosis, and matrix metalloproteinase (MMP) expression via the mitogen-activated protein kinase (MAPK) signaling pathway on L929 fibroblasts irradiated with UVB. DHCA exhibited high antioxidant capacity on 2,2-diphenyl-1-picrylhydrazyl (DPPH<jats:sup>•</jats:sup>), 2,2-azinobis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS<jats:sup>•+</jats:sup>), and xanthine/luminol/xanthine oxidase (XOD) assays and reduced UVB-induced cell death in the neutral red assay. DHCA also modulated oxidative stress by decreasing intracellular reactive oxygen species (ROS) and extracellular hydrogen peroxide (H<jats:sub>2</jats:sub>O<jats:sub>2</jats:sub>) production, enhancing catalase (CAT) and superoxide dismutase (SOD) activities and reduced glutathione (GSH) levels. Hence, cellular damage was attenuated by DHCA, including lipid peroxidation, apoptosis/necrosis and its markers (loss of mitochondria membrane potential, DNA condensation, and cleaved caspase 9 expression), and MMP-1 expression. Furthermore, DHCA reduced the phosphorylation of MAPK p38. These findings suggest that DHCA can be used in the development of skin care products to prevent UVB-induced skin damage.</jats:p>

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