Dieckol, an Algae-Derived Phenolic Compound, Suppresses UVB-Induced Skin Damage in Human Dermal Fibroblasts and Its Underlying Mechanisms

Lei Wang,Hye-Won Yang,You-Jin Jeon,Jun-Geon Je,Seungheon Lee

doi:10.3390/antiox10030352

Lei Wang, Hye-Won Yang + Show 3 more

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https://doi.org/10.3390/antiox10030352

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Journal: Antioxidants	Publication Date: Feb 26, 2021
Citations: 19	License type: CC BY 4.0

Affiliation: Jeju National University, Ocean University of China

Abstract

Ultraviolet (UV) irradiation is considered to be the primary environmental factor that causes skin damage. In the present study, we investigated the protective effect of dieckol (DK), a compound isolated from the brown seaweed Ecklonia cava, against UVB-induced skin damage in human dermal fibroblasts (HDF cells). The results indicated that DK effectively inhibited the activity of collagenase. DK remarkably reduced the intracellular reactive oxygen species level and improved the viability of UVB-irradiated HDF cells. Besides, DK significantly and dose-dependently improved collagen synthesis and inhibited intracellular collagenase activity in UVB-irradiated HDF cells. In addition, DK markedly reduced the expression of proinflammatory cytokines and matrix metalloproteinases. Further analyses revealed that these processes were mediated through the regulation of nuclear factor kappa B, activator protein 1, and mitogen-activated protein kinase signaling pathways in the UVB-irradiated HDF cells. In conclusion, these results indicate that DK possesses strong in vitro photoprotective effects and therefore has the potential to be used as an ingredient in the cosmeceutical industry.

Highlights

The levels of activated MAPKs were markedly and dose-dependently decreased in cells treated with DK (Figure 7). These results demonstrate that DK attenuates UVB-induced matrix metalloproteinases (MMPs) and pro-inflammatory cytokine expression in HDF cells by regulating AP-1, NF-κB, and MAPKs pathways
The collagen synthesis level in DK-treated HDF cells was markedly increased in a dose-dependent manner (Figure 3A). These results demonstrate that DK protects the skin against UVB-mediated inhibition of collagen synthesis, and inhibits collagen degradation by reducing the relative intracellular collagenase activity in UVB-irradiated
DK markedly attenuated the expression of these pro-inflammatory cytokines in the UVB-irradiated HDF cells in a dose-dependent manner. These results indicate that DK effectively inhibited collagen degradation and inflammatory response stimulated by UVB irradiation by reducing the expression of MMPs and pro-inflammatory cytokines in HDF cells

Summary

Introduction

Skin is the largest organ in the human body and directly exposed to the outside environment. The skin is constantly exposed to solar ultraviolet (UV) irradiation during normal daily life activities. Overexposure to UV irradiation leads to skin damage and diseases, such as edema, hyperpigmentation, erythema, sunburn, and cancer [1,2]. Previous studies have reported UVB-induced skin diseases and damage mainly by stimulating the expression of proinflammatory cytokines and matrix metalloproteinases (MMPs) by inducing overproduction of intracellular reactive oxygen species (ROS) [4,5]. An antioxidant agent that possesses strong ROS scavenging effect may be a potential candidate for the development of a therapeutic drug or cosmetic for the treatment of UVB-induced skin damage. Given that natural products have several advantages such as strong activity and low or no adverse effects, the discovery of ingredients from natural resources has attracted considerable research interest

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