ReferenceID 1786

Diosmin restores the skin barrier by targeting the aryl hydrocarbon receptor in atopic dermatitis

Phytomedicine

BACKGROUND: Atopic dermatitis (AD) is an inflammatory chronic skin disease that is characterized by the dysfunction or lack of skin barrier proteins. Recent studies have proposed that the pharmacological upregulation of

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Reference Id
1786
Evidence Id
18376
Core Evidence Id
18376
Source Reference Id
3564
Herb2 Reference Id
HBREF004361
Subject Paper Key
HBIN024193_33302042
Pubmed Id
33302042
Doi
10.1016/j.phymed.2020.153418
Paper Title
Diosmin restores the skin barrier by targeting the aryl hydrocarbon receptor in atopic dermatitis
Paper Abstract
BACKGROUND: Atopic dermatitis (AD) is an inflammatory chronic skin disease that is characterized by the dysfunction or lack of skin barrier proteins. Recent studies have proposed that the pharmacological upregulation of skin barrier proteins is an effective treatment for AD. Aryl hydrocarbon receptor (AhR) is a transcription factor that positively regulates the expression of skin barrier proteins upon its activation. PURPOSE: This study aimed to identify AhR agonists from phytochemicals and investigate its effect on skin barrier restoration as well as its mechanisms of action in AD. STUDY DESIGN: A publicly available assay database and HaCaT cells stably transduced with a luciferase gene driven by an AhR-target gene promoter (CYP1A1) were used to screen for the activity of AhR agonists from phytochemicals. Normal human epidermal keratinocytes (NHEKs) and a human skin equivalent (HSE) model were used to investigate the effect of AhR agonists on skin restoration and its underlying mechanisms. METHODS: A Gaussia luciferase assaywas performed to screen for AhR agonist activity. Western blotting, qRT-PCR analysis, immunofluorescence, drug affinity responsive target stability assay, and siRNA-mediated AhR knockdown were performed in NHEKs. Hematoxylin and eosin staining was performed to measure epidermal thickness in the HSE model. RESULTS: Diosmin, a potential AhR agonist derived from natural products, upregulated the expression of skin barrier proteins (filaggrin and loricrin) and their upstream regulator (OVOL1) in NHEKs. Diosmin treatment also increased epidermal thickness in the HSE model. In addition, incubating NHEKs with diosmin restored the expression of skin barrier proteins and mRNAs that were suppressed by Th2 cytokines and inhibited STAT3 phosphorylation that was induced by Th2 cytokines. Diosmin also upregulated the expression of NQO1, a negative regulator of STAT3. Immunofluorescence results showed that diosmin stimulated AhR nuclear translocation, and the drug affinity responsive target stability assay revealed that this phytochemical directly bound to AhR. Furthermore, AhR knockdown abolished diosmin-induced filaggrin and loricrin expression. CONCLUSION: These results suggest that diosmin is a potential treatment for AD that targets AhR.
Journal
Phytomedicine
Publish Year
2021
Experiment Subject
human; hacat cells
Experiment Type
Cell Experiment
Phenotype Related
Atopic Dermatitis; Inflammatory Chronic Skin Disease
Paper Title Cn
Paper Title En
Diosmin restores the skin barrier by targeting the aryl hydrocarbon receptor in atopic dermatitis
Bilingual Status
semi_complete