Pretreatment of Ferulic Acid Protects Human Dermal Fibroblasts against Ultraviolet A Irradiation.
- Author:
Hyung Jin HAHN
1
;
Ki Bbeum KIM
;
Seunghee BAE
;
Byung Gon CHOI
;
Sungkwan AN
;
Kyu Joong AHN
;
Su Young KIM
Author Information
- Publication Type:Original Article
- Keywords: Cell aging; DNA repair; Ferulic acid; Reactive oxygen species; Ultraviolet rays
- MeSH: Aging; Animals; Antioxidants; Catalase; Cats; Cell Aging; Cell Cycle; Cell Cycle Checkpoints; Cell Death; Complement System Proteins; DNA Repair; Fibroblasts*; Humans*; Luciferases; Matrix Metalloproteinase 1; Oxidative Stress; Reactive Oxygen Species; Real-Time Polymerase Chain Reaction; RNA, Messenger; Skin Aging; Superoxide Dismutase; Ultraviolet Rays; Xeroderma Pigmentosum
- From:Annals of Dermatology 2016;28(6):740-748
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Approximately 90%~99% of ultraviolet A (UVA) ray reaches the Earth's surface. The deeply penetrating UVA rays induce the formation of reactive oxygen species (ROS), which results in oxidative stress such as photoproducts, senescence, and cell death. Thus, UVA is considered a primary factor that promotes skin aging. OBJECTIVE: Researchers investigated whether pretreatment with ferulic acid protects human dermal fibroblasts (HDFs) against UVA-induced cell damages. METHODS: HDF proliferation was analyzed using the water-soluble tetrazolium salt assay. Cell cycle distribution and intracellular ROS levels were assessed by flow cytometric analysis. Senescence was evaluated using a senescence-associated β-galactosidase assay, while Gadd45α promoter activity was analyzed through a luciferase assay. The expression levels of superoxide dismutase 1 (SOD1), catalase (CAT), xeroderma pigmentosum complementation group A and C, matrix metalloproteinase 1 and 3, as well as p21 and p16 were measured using quantitative real-time polymerase chain reaction. RESULTS: Inhibition of proliferation and cell cycle arrest were detected in cells that were irradiated with UVA only. Pretreatment with ferulic acid significantly increased the proliferation and cell cycle progression in HDFs. Moreover, ferulic acid pretreatment produced antioxidant effects such as reduced DCF intensity, and affected SOD1 and CAT mRNA expression. These effects were also demonstrated in the analysis of cell senescence, promoter activity, expression of senescent markers, and DNA repair. CONCLUSION: These results demonstrate that ferulic acid exerts protective effects on UVA-induced cell damages via anti-oxidant and stress-inducible cellular mechanisms in HDFs.
