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

• Published in: Oxidative medicine and cellular longevity Vol. 2019; no. 2019; pp. 1 - 14
• Main Authors: Nakamura, Celso Vataru, Ueda-Nakamura, Tânia, Truiti, Maria da Conceição Torrado, Silva, Sueli de Oliveira, Daré, Regina G., Ratti, Bianca Altrão, Oliveira, Mariana M., Auzely, Rachel
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2019; Hindawi; Hindawi Limited
• Subjects: Acids; Animals; Antioxidants - pharmacology; Apoptosis; Apoptosis - drug effects; Apoptosis - radiation effects; Caffeic Acids - chemistry; Caffeic Acids - pharmacology; Cell Line; Cell Survival - drug effects; Cell Survival - radiation effects; Cytoprotection - drug effects; Cytoprotection - radiation effects; Ethanol; Fibroblasts; Kinases; Laboratories; Lipid peroxidation; Lipid Peroxidation - drug effects; Lipid Peroxidation - radiation effects; MAP Kinase Signaling System - drug effects; MAP Kinase Signaling System - radiation effects; Matrix Metalloproteinase 1 - metabolism; Membrane Potential, Mitochondrial - drug effects; Membrane Potential, Mitochondrial - radiation effects; Mice; Oxidative stress; Oxidative Stress - drug effects; Oxidative Stress - radiation effects; p38 Mitogen-Activated Protein Kinases - metabolism; Phosphorylation - drug effects; Phosphorylation - radiation effects; Polyphenols; Proteins; Reactive oxygen species; Reactive Oxygen Species - metabolism; Signal transduction; Ultraviolet Rays; United States > US; Grand Island New York
• DOI: 10.1155/2019/2419096
• ISSN: 1942-0900

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•), 2,2-azinobis-3-ethylbenzothiazoline-6-sulphonic acid (ABTS•+), 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 (H2O2) 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.