Suppr超能文献

没食子酸对紫外线照射的成纤维细胞和无毛小鼠的皮肤光老化具有调节作用。

Gallic acid regulates skin photoaging in UVB-exposed fibroblast and hairless mice.

作者信息

Hwang Eunson, Park Sang-Yong, Lee Hyun Ji, Lee Tae Youp, Sun Zheng-Wang, Yi Tae Hoo

机构信息

Department of Oriental Medicinal Material and Processing, College of Life Science, Kyung Hee University, Global Campus, 1732 Deokyoungdaero, Giheung-gu, Yongin-si, Gyeonggi-do, 446-701, Korea.

出版信息

Phytother Res. 2014 Dec;28(12):1778-88. doi: 10.1002/ptr.5198. Epub 2014 Aug 8.

Abstract

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-β1. Our data indicate that GA is a potential candidate for the prevention of UVB-induced premature skin aging.

摘要

紫外线(UV)辐射是皮肤光老化的主要因素,其特征为皱纹形成、皮肤干燥和增厚。皮肤光老化的潜在机制与基质金属蛋白酶(MMP)活性上调导致的胶原蛋白降解密切相关,而MMP活性上调是由活性氧(ROS)生成所诱导的。没食子酸(GA)是一种酚类化合物,具有多种生物活性,包括抗氧化和抗炎活性。我们使用正常人皮肤成纤维细胞(NHDFs)在体外以及无毛小鼠在体内研究了GA对紫外线B(UVB)照射引起的光老化的保护作用。在UVB照射并经GA处理的NHDFs中,ROS、白细胞介素-6和MMP-1的产生水平显著受到抑制,并且I型前胶原的表达受到刺激。GA处理抑制了转录因子活化蛋白1的活性。通过测量皱纹形成、组织学改变、蛋白质表达以及诸如角质层水合作用、经表皮水分流失和红斑指数等生理变化,研究了GA局部应用和饮食给药后的效果。我们发现,GA通过负向调节MMP-1分泌以及正向调节弹性蛋白、I型前胶原和转化生长因子-β1,减少了皮肤干燥、厚度和皱纹形成。我们的数据表明,GA是预防UVB诱导的皮肤过早老化的潜在候选物。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验