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烟草烟雾诱导皮肤过早老化的分子基础。

Molecular basis of tobacco smoke-induced premature skin aging.

作者信息

Morita Akimichi, Torii Kan, Maeda Akira, Yamaguchi Yuji

机构信息

Department of Geriatric and Environmental Dermatology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.

出版信息

J Investig Dermatol Symp Proc. 2009 Aug;14(1):53-5. doi: 10.1038/jidsymp.2009.13.

DOI:10.1038/jidsymp.2009.13
PMID:19675554
Abstract

Although it is now widely recognized that tobacco smoke has negative effects on the skin, the molecular mechanisms underlying its skin-aging effects remain uncertain. Epidemiological studies indicate that tobacco smoking is a strong independent predictor of facial wrinkle formation and other aspects of premature skin aging. Recent in vivo studies in humans and mice provided the first direct evidence that tobacco smoke causes premature skin aging, and they have begun to reveal the molecular changes in the skin that occur in response to it. Water-soluble tobacco smoke extract, which predominantly produces oxidative stress when applied topically to cultured skin fibroblasts, impairs collagen biosynthesis. Matrix metalloproteinases, which degrade collagen, are induced dose-dependently by tobacco smoke extract as well as by other constituents that trigger the aryl hydrocarbon receptor (AhR), a ligand-dependent transcription factor that mediates the toxicity of several environmental contaminants, including photoproducts in the body generated by UVB radiation. Tobacco smoke also contains many non-water-soluble constituents that activate the AhR pathway. Our most recent studies using hexane-soluble tobacco extract indicate that activation of the AhR pathway may play a role in the premature skin-aging effects of tobacco smoke exposure.Journal of Investigative Dermatology Symposium Proceedings (2009) 14, 53-55; doi:10.1038/jidsymp.2009.13.

摘要

尽管现在人们普遍认识到烟草烟雾对皮肤有负面影响,但其导致皮肤老化的分子机制仍不明确。流行病学研究表明,吸烟是面部皱纹形成和皮肤过早老化其他方面的一个强有力的独立预测因素。最近在人类和小鼠身上进行的体内研究提供了首个直接证据,证明烟草烟雾会导致皮肤过早老化,并且这些研究已开始揭示皮肤中因烟草烟雾而发生的分子变化。水溶性烟草烟雾提取物在局部应用于培养的皮肤成纤维细胞时主要产生氧化应激,会损害胶原蛋白的生物合成。降解胶原蛋白的基质金属蛋白酶会被烟草烟雾提取物以及其他触发芳烃受体(AhR)的成分剂量依赖性地诱导,AhR是一种配体依赖性转录因子,介导包括紫外线B辐射在体内产生的光产物在内的几种环境污染物的毒性。烟草烟雾还含有许多激活AhR途径的非水溶性成分。我们最近使用己烷可溶性烟草提取物进行的研究表明,AhR途径的激活可能在接触烟草烟雾导致的皮肤过早老化效应中起作用。《皮肤病学研究杂志》研讨会论文集(2009年)14卷,53 - 55页;doi:10.1038/jidsymp.2009.13

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