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抗氧化植物化学物质通过 AHR-OVOL1 通路加速表皮终末分化:对特应性皮炎的影响。

Antioxidative Phytochemicals Accelerate Epidermal Terminal Differentiation via the AHR-OVOL1 Pathway: Implications for Atopic Dermatitis.

机构信息

Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, 812-8582 Fukuoka, Japan.

出版信息

Acta Derm Venereol. 2018 Nov 5;98(10):918-923. doi: 10.2340/00015555-3003.

DOI:10.2340/00015555-3003
PMID:29972223
Abstract

Aryl hydrocarbon receptor (AHR) is a chemical sensor that is expressed abundantly in epidermal keratinocytes. Oxidative AHR ligands induce the production of reactive oxygen species. However, antioxidant AHR ligands inhibit reactive oxygen species generation via activation of nuclear factor-erythroid 2-related factor-2, which is a master switch for antioxidative signalling. In addition, AHR signalling accelerates epidermal terminal differentiation, but excessive acceleration by oxidative ligands, such as dioxins, may induce chloracne and inflammation. However, antioxidative phytochemical ligands induce the beneficial acceleration of epidermal differentiation that repairs skin barrier disruption. The upregulated expression of differentiation molecules, such as filaggrin, is mediated via the AHR-OVOL1 axis. This AHR-OVOL1 system is capable of counteracting skin barrier dysfunction in T-helper type 2-shifted inflammation. This article reviews the dynamic and multifaceted role of AHR in epidermal biology and discusses the potential use of antioxidative phytochemical ligands for AHR in inflammatory skin diseases, such as atopic dermatitis.

摘要

芳香烃受体 (AHR) 是一种化学感受器,在表皮角质形成细胞中大量表达。氧化 AHR 配体诱导活性氧的产生。然而,抗氧化 AHR 配体通过激活核因子红细胞 2 相关因子 2 抑制活性氧的产生,核因子红细胞 2 相关因子 2 是抗氧化信号的主要开关。此外,AHR 信号加速表皮终末分化,但氧化配体(如二恶英)的过度加速可能诱导氯痤疮和炎症。然而,抗氧化植物化学配体诱导有益的表皮分化加速,修复皮肤屏障破坏。分化分子(如丝聚合蛋白)的上调表达是通过 AHR-OVOL1 轴介导的。该 AHR-OVOL1 系统能够对抗 T 辅助细胞 2 型炎症转移引起的皮肤屏障功能障碍。本文综述了 AHR 在表皮生物学中的动态和多方面作用,并讨论了抗氧化植物化学配体在特应性皮炎等炎症性皮肤病中 AHR 的潜在用途。

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