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抗氧化剂白头翁提取物通过AHR/OVOL1途径增强丝聚合蛋白和兜甲蛋白的表达。

Antioxidant Artemisia princeps Extract Enhances the Expression of Filaggrin and Loricrin via the AHR/OVOL1 Pathway.

作者信息

Hirano Akiko, Goto Masashi, Mitsui Tsukasa, Hashimoto-Hachiya Akiko, Tsuji Gaku, Furue Masutaka

机构信息

Beauty Care R&D, Health & Beauty Company, Sunstar Group, Kamihamuro 5-30-1, Takatsuki, Osaka 569-1044, Japan.

Department of Dermatology, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan.

出版信息

Int J Mol Sci. 2017 Sep 11;18(9):1948. doi: 10.3390/ijms18091948.

Abstract

The Japanese mugwort, ( in Japanese), has anti-inflammatory and antioxidant effects. Skin care products containing extract (APE) are known to improve dry skin symptoms in atopic dermatitis. Atopic dry skin is associated with a marked reduction of skin barrier proteins, such as filaggrin (FLG) and loricrin (LOR). Recently, aryl hydrocarbon receptor (AHR), and its downstream transcription factor OVO-like 1 (OVOL1), have been shown to regulate the gene expression of FLG and LOR. The focus of this paper is to evaluate the effects of APE on the AHR/OVOL1/FLG or LOR pathway since they have remained unknown to this point. We first demonstrated that non-cytotoxic concentrations of APE significantly upregulated antioxidant enzymes, NAD(P)H dehydrogenase quinone 1 and heme oxygenase 1, in human keratinocytes. Even at these low concentrations, APE induced nuclear translocation of AHR and significantly upregulated (a specific target gene for AHR activation), , and expression. AHR knockdown downregulated expression. The APE-induced upregulation of and was canceled in keratinocytes with AHR or OVOL1 knockdown. In conclusion, antioxidant APE is a potent phytoextract that upregulates and expression in an AHR/OVOL1-dependent manner and this may underpin the barrier-repairing effects of APE in treating atopic dry skin.

摘要

日本艾蒿(日语中称为 )具有抗炎和抗氧化作用。已知含有日本艾蒿提取物(APE)的护肤品可改善特应性皮炎中的干性皮肤症状。特应性干性皮肤与皮肤屏障蛋白如丝聚合蛋白(FLG)和兜甲蛋白(LOR)的显著减少有关。最近,芳烃受体(AHR)及其下游转录因子OVO样蛋白1(OVOL1)已被证明可调节FLG和LOR的基因表达。本文的重点是评估APE对AHR/OVOL1/FLG或LOR途径的影响,因为到目前为止这些影响尚不清楚。我们首先证明,非细胞毒性浓度的APE可显著上调人角质形成细胞中的抗氧化酶NAD(P)H脱氢酶醌1和血红素加氧酶1。即使在这些低浓度下,APE也会诱导AHR的核转位,并显著上调 (AHR激活的特定靶基因)、 和 的表达。AHR敲低会下调 的表达。在AHR或OVOL1敲低的角质形成细胞中,APE诱导的 和 的上调被消除。总之,抗氧化剂APE是一种有效的植物提取物,它以AHR/OVOL1依赖的方式上调 和 的表达,这可能是APE治疗特应性干性皮肤时屏障修复作用的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b640/5618597/51c60b69c583/ijms-18-01948-g001.jpg

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