Gallic Acid Regulates Skin Photoaging in UVB-exposed Fibroblast and Hairless Mice

被引:126
作者
Hwang, Eunson [1 ]
Park, Sang-Yong [1 ]
Lee, Hyun Ji [1 ]
Lee, Tae Youp [1 ]
Sun, Zheng-wang [1 ]
Yi, Tae Hoo [1 ]
机构
[1] Kyung Hee Univ, Coll Life Sci, Dept Oriental Med Mat & Proc, Yongin 446701, Gyeonggi Do, South Korea
关键词
gallic acid; photoaging; ROS; MMP-1; type I procollagen; hairless mice; OXIDATIVE STRESS; COLLAGENASE; DAMAGE; MMP-1; IRRADIATION; MECHANISMS; INDUCTION; RATS;
D O I
10.1002/ptr.5198
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Ultraviolet (UV) radiation is the primary factor in skin photoaging, which is characterized by wrinkle formation, dryness, and thickening. The mechanisms underlying skin photoaging are closely associated with degradation of collagen via upregulation of matrix metalloproteinase (MMP) activity, which is induced by reactive oxygen species (ROS) production. Gallic acid (GA), a phenolic compound, possesses a variety of biological activities including antioxidant and antiinflammatory activities. We investigated the protective effects of GA against photoaging caused by UVB irradiation using normal human dermal fibroblasts (NHDFs) in vitro and hairless mice in vivo. The production levels of ROS, interlukin-6, and MMP-1 were significantly suppressed, and type I procollagen expression was stimulated in UVB-irradiated and GA-treated NHDFs. GA treatment inhibited the activity of transcription factor activation protein 1. The effects of GA following topical application and dietary administration were examined by measuring wrinkle formation, histological modification, protein expression, and physiological changes such as stratum corneum hydration, transepidermal water loss, and erythema index. We found that GA decreased dryness, skin thickness, and wrinkle formation via negative modulation of MMP-1 secretion and positive regulation of elastin, type I procollagen, and transforming growth factor-1. Our data indicate that GA is a potential candidate for the prevention of UVB-induced premature skin aging. Copyright (c) 2014 John Wiley & Sons, Ltd.
引用
收藏
页码:1778 / 1788
页数:11
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