Antioxidant artemisia princeps extract enhances the expression of Filaggrin and Loricrin via the AHR/OVOL1 pathway

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

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The Japanese mugwort, Artemisia princeps (yomogi in Japanese), has anti-inflammatory and antioxidant effects. Skin care products containing Artemisia princeps 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 CYP1A1 (a specific target gene for AHR activation), FLG, and LOR expression. AHR knockdown downregulated OVOL1 expression. The APE-induced upregulation of FLG and LOR was canceled in keratinocytes with AHR or OVOL1 knockdown. In conclusion, antioxidant APE is a potent phytoextract that upregulates FLG and LOR expression in an AHR/OVOL1-dependent manner and this may underpin the barrier-repairing effects of APE in treating atopic dry skin.

Original languageEnglish
Article numberA1948
JournalInternational journal of molecular sciences
Volume18
Issue number9
DOIs
Publication statusPublished - Sep 11 2017

Fingerprint

Artemisia
Aryl Hydrocarbon Receptors
antioxidants
Antioxidants
hydrocarbons
Hydrocarbons
Skin
Skin care products
Keratinocytes
dermatitis
NAD(P)H Dehydrogenase (Quinone)
Up-Regulation
Cytochrome P-450 CYP1A1
Heme Oxygenase-1
Transcription factors
dehydrogenases
gene expression
quinones
Skin Care
filaggrin

All Science Journal Classification (ASJC) codes

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

Cite this

Antioxidant artemisia princeps extract enhances the expression of Filaggrin and Loricrin via the AHR/OVOL1 pathway. / Hirano, Akiko; Goto, Masashi; Mitsui, Tsukasa; Hashimoto-Hachiya, Akiko; Tsuji, Gaku; Furue, Masutaka.

In: International journal of molecular sciences, Vol. 18, No. 9, A1948, 11.09.2017.

Research output: Contribution to journalArticle

@article{3a130348ba6641599f8b1ce0fbb38e0b,
title = "Antioxidant artemisia princeps extract enhances the expression of Filaggrin and Loricrin via the AHR/OVOL1 pathway",
abstract = "The Japanese mugwort, Artemisia princeps (yomogi in Japanese), has anti-inflammatory and antioxidant effects. Skin care products containing Artemisia princeps 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 CYP1A1 (a specific target gene for AHR activation), FLG, and LOR expression. AHR knockdown downregulated OVOL1 expression. The APE-induced upregulation of FLG and LOR was canceled in keratinocytes with AHR or OVOL1 knockdown. In conclusion, antioxidant APE is a potent phytoextract that upregulates FLG and LOR expression in an AHR/OVOL1-dependent manner and this may underpin the barrier-repairing effects of APE in treating atopic dry skin.",
author = "Akiko Hirano and Masashi Goto and Tsukasa Mitsui and Akiko Hashimoto-Hachiya and Gaku Tsuji and Masutaka Furue",
year = "2017",
month = "9",
day = "11",
doi = "10.3390/ijms18091948",
language = "English",
volume = "18",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "9",

}

TY - JOUR

T1 - Antioxidant artemisia princeps extract enhances the expression of Filaggrin and Loricrin via the AHR/OVOL1 pathway

AU - Hirano, Akiko

AU - Goto, Masashi

AU - Mitsui, Tsukasa

AU - Hashimoto-Hachiya, Akiko

AU - Tsuji, Gaku

AU - Furue, Masutaka

PY - 2017/9/11

Y1 - 2017/9/11

N2 - The Japanese mugwort, Artemisia princeps (yomogi in Japanese), has anti-inflammatory and antioxidant effects. Skin care products containing Artemisia princeps 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 CYP1A1 (a specific target gene for AHR activation), FLG, and LOR expression. AHR knockdown downregulated OVOL1 expression. The APE-induced upregulation of FLG and LOR was canceled in keratinocytes with AHR or OVOL1 knockdown. In conclusion, antioxidant APE is a potent phytoextract that upregulates FLG and LOR expression in an AHR/OVOL1-dependent manner and this may underpin the barrier-repairing effects of APE in treating atopic dry skin.

AB - The Japanese mugwort, Artemisia princeps (yomogi in Japanese), has anti-inflammatory and antioxidant effects. Skin care products containing Artemisia princeps 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 CYP1A1 (a specific target gene for AHR activation), FLG, and LOR expression. AHR knockdown downregulated OVOL1 expression. The APE-induced upregulation of FLG and LOR was canceled in keratinocytes with AHR or OVOL1 knockdown. In conclusion, antioxidant APE is a potent phytoextract that upregulates FLG and LOR expression in an AHR/OVOL1-dependent manner and this may underpin the barrier-repairing effects of APE in treating atopic dry skin.

UR - http://www.scopus.com/inward/record.url?scp=85029374916&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85029374916&partnerID=8YFLogxK

U2 - 10.3390/ijms18091948

DO - 10.3390/ijms18091948

M3 - Article

C2 - 28892018

AN - SCOPUS:85029374916

VL - 18

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1661-6596

IS - 9

M1 - A1948

ER -