23-Hydroxytormentic acid protects human dermal fibroblasts by attenuating UVA-induced oxidative stress

Autor: Ki Bbeum Kim, In-Sook An, Kyu Joong Ahn, Hae Jeong Youn, Hyo-Sun Han
Rok vydání: 2017
Předmět:
0301 basic medicine
Antioxidant
Photoaging
medicine.medical_treatment
Interleukin-1beta
Gene Expression
medicine.disease_cause
Antioxidants
0302 clinical medicine
Gene expression
Immunology and Allergy
Cells
Cultured
Cellular Senescence
chemistry.chemical_classification
General Medicine
Dermis
Catalase
medicine.anatomical_structure
030220 oncology & carcinogenesis
Matrix Metalloproteinase 1
DNA damage
Cell Survival
NF-E2-Related Factor 2
Ultraviolet Rays
Immunology
Dermatology
Biology
Collagen Type I
03 medical and health sciences
Picrates
medicine
Humans
Radiology
Nuclear Medicine and imaging
Viability assay
Benzothiazoles
RNA
Messenger
Fibroblast
Reactive oxygen species
Glutathione Peroxidase
Interleukin-6
Tumor Necrosis Factor-alpha
Biphenyl Compounds
Hydrogen Peroxide
Fibroblasts
medicine.disease
Molecular biology
Triterpenes
Collagen Type I
alpha 1 Chain
Oxidative Stress
030104 developmental biology
chemistry
Sulfonic Acids
Reactive Oxygen Species
Oxidative stress
Heme Oxygenase-1
Zdroj: Photodermatology, photoimmunologyphotomedicine. 33(2)
ISSN: 1600-0781
Popis: Ultraviolet A (UVA), one of the major components of sunlight, can penetrate the dermal layer of the skin and generate reactive oxygen species (ROS). It causes alterations in the dermal connective tissue and gene expression, inflammation, photoaging, and DNA damage. Therefore, the harmful effects of UVA and strategies to reduce it have been consistently investigated. 23-Hydroxytormentic acid (23-HTA) has been demonstrated to improve drug-induced nephrotoxicity and exhibit several free radical scavenging effects with other molecules. Therefore, the aim of this study was to investigate the anti-inflammatory effects and extracellular matrix (ECM) reconstructive activity of 23-HTA in UVA-irradiated normal human dermal fibroblasts (NHDFs). The antioxidant capacity of 23-HTA was determined by examining its scavenging activities against hydrogen peroxide, 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid), and diphenylpicrylhydrazyl in vitro. Its effect on cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tertazolium bromide, and 2,7-dichlorofluorescin diacetate was used to investigate intracellular ROS scavenging activity. The mRNA levels of antioxidant enzymes and pro-inflammatory cytokines were detected using quantitative real-time polymerase chain reaction. A senescence-associated β-galactosidase (SA-β-gal) staining kit was used to assess senescent cells. 23-HTA showed antioxidant capacity mediated by ROS scavenging and regulation of antioxidant-related gene expression. Further, the SA-β-gal analysis and mRNA expression of matrix metalloproteinases and type I procollagen suggested that 23-HTA regulates the gene expression of ECM proteins and cellular senescence under UVA-irradiated conditions. In conclusion, 23-HTA protects against and attenuates UVA-induced oxidative stress in NHDFs likely via the nuclear factor erythroid-derived 2-like 2 signaling pathway. This article is protected by copyright. All rights reserved.
Databáze: OpenAIRE
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