Pretreatment of Ferulic Acid Protects Human Dermal Fibroblasts against Ultraviolet A Irradiation

Abstract

BackgroundApproximately 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.ObjectiveResearchers investigated whether pretreatment with ferulic acid protects human dermal fibroblasts (HDFs) against UVA-induced cell damages.MethodsHDF 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.ResultsInhibition 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.ConclusionThese results demonstrate that ferulic acid exerts protective effects on UVA-induced cell damages via anti-oxidant and stress-inducible cellular mechanisms in HDFs.

Antioxidant Properties of Ferulic Acid and Its Possible Application

“…It prevents UV-induced cell cycle alterations and DNA damage and regulates the expression of DNA repair genes. Hahn and partners [19] have shown that intracellular ROS production is nearly 2-fold lower in fibroblasts, which after irradiation with UVA, have ferulic acid applied. Similar effects, in the form of protection against free radical damage, have been observed in UVBexposed fibroblasts.…”

Fluorofenidone inhibits UV‐A induced senescence in human dermal fibroblasts via the mammalian target of rapamycin‐dependent SIRT1 pathway

“…UV-A photons can induce fibroblasts to synthesize metalloproteinase 1, which stimulates degradation of the collagenous extracellular matrix and accounts for most of the connective tissue damage. 27,28 Cellular senescence of human skin fibroblasts has been reported as one of the most important causes of skin aging. 29 UV-A can induce senescence of human skin fibroblasts which will lead to loose, fragile of skin appearance and account for skin aging.…”

Salmon nasal cartilage proteoglycan enhances growth of normal human dermal fibroblast through Erk1/2 phosphorylation

“…Because dermal fibroblasts represent the main cellular component of the dermis and are responsible for the production and the homeostatic maintenance of skin extracellular matrix, [21][22][23] it is inferred that the inhibition of dermal fibroblast proliferation by increased production of reactive oxygen species due to aging or ultraviolet light leads to the disruption of skin homeostasis. [24][25][26][27] Furthermore, because it has been reported that Salmon-PG is absorbed by the rat jejunum and ileum, absorbed Salmon-PG may pass from the systemic circulation into dermis and has an effect on proliferation of dermal fibroblasts. Thus, this finding suggests that Salmon-PG may contribute to the maintenance of skin homeostasis.…”