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Background Hydroxytyrosol is discovered in a form of elenolic acid ester oleuropein in olive leaf and oil. The anti-carcinogenic, antioxidant, and anti-inflammatory effects of hydroxytyrosol have been reported in the food, medical, pharmaceutical, and life science fields. But it has not been studied on skin biology field. This study is demonstrated using UVA-induced cellular aging model of human dermal fibroblast. Methods The cell survival rate was measured using the principle of water-soluble tetrazolium salt-1 assay, which is a measurement method for cell survival rate. The quantitative real-time PCR (qRT-PCR) was used to quantitatively analyze the gene expression changes in human dermal fibroblasts (HDFs) by hydroxytyrosol. Senescence-associated β-galactosidase (SA-β-gal) assay was implemented to dye β-galactosidases (used as a cell aging biomarker) to measure HDF cell aging by UVA. Results Hydroxytyrosol decreased the SA-β-galactosidase activity in a dose-dependent manner in UVA-exposed HDFs. Also, the elevated expression of MMP-1 and MMP-3 by UVA were decreased by hydroxytyrosol in a dose-dependent manner. To examine the anti-inflammatory effect of hydroxytyrosol in UV exposed HDFs, the expression of inflammatory interleukins IL-1β, IL-6, and IL-8 were analyzed. Quantitative RT-PCR showed that hydroxytyrosol decreased the expression of IL-1β, IL-6, and IL-8 gene. Conclusion Through this research, we demonstrate that hydroxytyrosol has effects on anti-inflammatory and anti-aging in HDFs damaged by UVA. We suggest that hydroxytyrosol is fully worthy of using as a cosmetic material effective to anti-inflammatory and to delay cellular senescence on HDFs.

Background Among various extra stimuli of humans, ultraviolet (UV) has been the most studied factor because it arouses not only internal but also external irritation in the body. UVA, one type of UV rays, has a wavelength between 320 and 400 nm and capacity to penetrate the skin dermal layer. Therefore, studies on how to reduce UVA-induced maleficence have been investigated vibrantly. Angelic acid has been demonstrated to aid in wound healing and exhibited sedative and psychotropic properties. But there have not been sufficient reports whether angelic acid has potential properties in the cosmeceutical aspect. Methods To investigate protective effects of angelic acid on UVA-induced oxidative stress and disruption of extracellular matrix, researchers analyzed cell proliferation rate, intracellular reactive oxygen species (ROS) scavenging capacity, cellular senescence, transcriptional activity of activating protein-1 (AP-1) transcription factor, and gene expression of antioxidant enzymes and connective tissue-related proteins. Results Pretreatment of angelic acid in normal human dermal fibroblasts (NHDFs) showed protective effect on UVA-induced proliferative inhibition. Via estimating ROS scavenging activity, angelic acid represented a scavenging effect of excessive increased intracellular ROS which is induced by UVA irradiation. Through quantitative real-time polymerase reaction, antioxidant enzyme and extracellular matrix (ECM)-related protein coded gene expressions were analyzed. Analysis of senescent cell and AP-1 promoter activity by beta-galactosidase assay and luciferase reporter gene assay, respectively, indicated how angelic acid regulates cellular mechanisms associated with connective tissue density. Conclusions Through the present study, researchers verify that angelic acid has dermal protective effect against UVA and suggest angelic acid as an efficacious cosmetic material preventing dermal cellular damages.