Abstract

A number of studies have demonstrated that marine carbohydrates display anti-oxidant, anti-melanogenic, and anti-aging activities in the skin. Laminarin (LA), a low-molecular-weight polysaccharide, is found in brown algae. The benefits of LA in ultraviolet B (UVB) induced photodamage of the skin have not been reported. The aim of this study was to investigate the effects of pre-treated LA on histopathological changes and oxidative damage in mouse dorsal skin on day 5, following repeated UVB exposure. Histopathology, Western blot analysis and immunohistochemical studies showed that epidermal thickness in the UVB group was significantly increased; however, the thickness in the UVB group treated with LA (LA/UVB group) was less compared with that of the UVB group. Collagen fibers in the dermis of the UVB group were significantly decreased and destroyed, whereas, in the LA/UVB group, the density of collagen fibers was significantly increased compared with that of the UVB group. Oxidative stress due to superoxide anion production measured via dihydroethidium fluorescence staining was dramatically increased in the UVB group, whereas in the LA/UVB group, the oxidative stress was significantly decreased. Expressions of SOD1, glutathione peroxidase and catalase were markedly reduced in the UVB group, whereas in the LA/UVB group, they were significantly higher along with SOD2 than in the control group. Taken together, our results indicate that LA pretreatment prevents or attenuates skin damage, by decreasing oxidative stress and increasing antioxidant enzymes in mouse dorsal skin.

Highlights

  • Skin is made up of two layers, the epidermis and dermis, and serves as an initial barrier against ultraviolet (UV) light, pathogens, and chemicals [1]

  • Exposure to UV radiation is the primary factor leading to the skin aging that is known as photoaging [17]

  • We investigated whether LA pretreatment, which has been reported to display antioxidant [19,20] and anti-aging activities [16], attenuates skin damage by reducing oxidative stress and increasing endogenous antioxidant levels in mouse dorsal skin following ultraviolet B (UVB) irradiation

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Summary

Introduction

Skin is made up of two layers, the epidermis and dermis, and serves as an initial barrier against ultraviolet (UV) light, pathogens, and chemicals [1]. Keratinocytes are the major cell type, which play important roles in the skin barrier by secreting various proteins and lipids [2]. Fibroblasts are the major cells in the dermis and mediate the synthesis and degradation of fibrous and non-fibrous matrix proteins [3]. Exposure to UV irradiation triggers an acute skin response, including sunburn (erythema), tanning (pigmentation), damage-related immunosuppression and epidermal hyperplasia [4]. Repeated exposure to UV generates excessive reactive oxygen species (ROS) and damages the enzymatic and non-enzymatic antioxidant defense systems in the skin, and results in the damage of cellular proteins, lipids and DNA [5,6]. UV exacerbates an inflammatory response in the skin by promoting and activating inflammatory cells, such as neutrophils, macrophages, mast cells which cause skin damage (photoaging) [5,6]

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