Abstract

Astaxanthin, a carotenoid found mainly in seafood, has potential clinical applications due to its antioxidant activity. In this study, we evaluated the effect of dietary astaxanthin derived from Haematococcus pluvialis on skin photoaging in UVA-irradiated hairless mice by assessing various parameters of photoaging. After chronic ultraviolet A (UVA) exposure, a significant increase in transepidermal water loss (TEWL) and wrinkle formation in the dorsal skin caused by UVA was observed, and dietary astaxanthin significantly suppressed these photoaging features. We found that the mRNA expression of lympho-epithelial Kazal-type-related inhibitor, steroid sulfatase, and aquaporin 3 in the epidermis was significantly increased by UVA irradiation for 70 days, and dietary astaxanthin significantly suppressed these increases in mRNA expression to be comparable to control levels. In the dermis, the mRNA expression of matrix metalloprotease 13 was increased by UVA irradiation and significantly suppressed by dietary astaxanthin. In addition, HPLC-PDA analysis confirmed that dietary astaxanthin reached not only the dermis but also the epidermis. Our results indicate that dietary astaxanthin accumulates in the skin and appears to prevent the effects of UVA irradiation on filaggrin metabolism and desquamation in the epidermis and the extracellular matrix in the dermis.

Highlights

  • The skin functions as the outermost barrier of the body and is in direct contact with the environment, which causes physical damage

  • After chronic ultraviolet A (UVA) exposure, a significant increase in transepidermal water loss (TEWL) by UVA was observed, and which demonstrated a trend toward suppression by dietary astaxanthin at 56 days

  • The mRNA expression of matrix metalloprotease 13 (MMP13) was increased by UVA irradiation, and this increase was significantly suppressed in the 0.1% astaxanthin group (Fig 8a)

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Summary

Introduction

The skin functions as the outermost barrier of the body and is in direct contact with the environment, which causes physical damage. Chronic exposure to ultraviolet (UV) radiation from the sun contributes to skin photoaging, which is clinically characterized by dryness, pigmentation, laxity, and deep wrinkling [3, 4]. UV radiation comprises wavelengths from 200 to 400 nm, and is further divided into three sections: UVA (320–400 nm), UVB (280–320 nm), and UVC (200–280 nm). UVC is filtered out by atmospheric ozone for the most part, both UVA and UVB radiation can reach the Earth’s surface and cause biological consequence to the skin [5, 6]. Exposure to UVB radiation is the primary cause of skin cancer in humans and animals [7]. Despite being weakly carcinogenic as PLOS ONE | DOI:10.1371/journal.pone.0171178 February 7, 2017

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