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

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 lo...

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Veröffentlicht in:International journal of molecular sciences 2017-09, Vol.18 (9), p.1948
Hauptverfasser: Hirano, Akiko, Goto, Masashi, Mitsui, Tsukasa, Hashimoto-Hachiya, Akiko, Tsuji, Gaku, Furue, Masutaka
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container_issue 9
container_start_page 1948
container_title International journal of molecular sciences
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creator Hirano, Akiko
Goto, Masashi
Mitsui, Tsukasa
Hashimoto-Hachiya, Akiko
Tsuji, Gaku
Furue, Masutaka
description 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.
doi_str_mv 10.3390/ijms18091948
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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. 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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. 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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.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>28892018</pmid><doi>10.3390/ijms18091948</doi><orcidid>https://orcid.org/0000-0002-2967-1073</orcidid><oa>free_for_read</oa></addata></record>
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subjects Antioxidants
Antioxidants - pharmacology
Aromatic compounds
Artemisia - chemistry
Atopic dermatitis
Basic Helix-Loop-Helix Transcription Factors - genetics
Basic Helix-Loop-Helix Transcription Factors - metabolism
Cell Line
Cytochrome P-450 CYP1A1 - genetics
Cytochrome P-450 CYP1A1 - metabolism
Cytochrome P450
Cytotoxicity
Dermatitis
DNA-Binding Proteins - genetics
DNA-Binding Proteins - metabolism
Filaggrin
Gene expression
Heme
Humans
Inflammation
Intermediate Filament Proteins - genetics
Intermediate Filament Proteins - metabolism
Keratinocytes
Keratinocytes - drug effects
Keratinocytes - metabolism
Low concentrations
Maintenance
Membrane Proteins - genetics
Membrane Proteins - metabolism
NADPH dehydrogenase
NADPH Dehydrogenase - genetics
NADPH Dehydrogenase - metabolism
Nuclear transport
Oxygenase
Plant Extracts - pharmacology
Proteins
Quinones
Receptors, Aryl Hydrocarbon - genetics
Receptors, Aryl Hydrocarbon - metabolism
Skin
Skin care products
Transcription Factors - genetics
Transcription Factors - metabolism
title Antioxidant Artemisia princeps Extract Enhances the Expression of Filaggrin and Loricrin via the AHR/OVOL1 Pathway
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