Aromatic oil from lavender as an atopic dermatitis suppressant

In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefo...

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Veröffentlicht in:PloS one 2024-01, Vol.19 (1), p.e0296408-e0296408
Hauptverfasser: Sato, Haruna, Kato, Kosuke, Koreishi, Mayuko, Nakamura, Yoshimasa, Tsujino, Yoshio, Satoh, Ayano
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creator Sato, Haruna
Kato, Kosuke
Koreishi, Mayuko
Nakamura, Yoshimasa
Tsujino, Yoshio
Satoh, Ayano
description In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines.
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Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. 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subjects Acetates
Acetic acid
Advertising executives
Air pollution
Analgesics
Animals
Antigens
Atopic dermatitis
Carbazole
Carbazoles
Care and treatment
Cell activation
Cosmetics
Cytokines
Dendritic cells
Dermatitis
Dermatitis, Atopic - drug therapy
Diagnosis
Dioxins
Essential oils
Esters
Folk medicine
Food preservation
Gene expression
Health aspects
Humans
Hydrocarbons
Immunoglobulins
Itching
Lavandula
Lavandula angustifolia
Lavender oil
Linalool
Linalyl acetate
Metabolites
Monoterpenes
Mutation
Nerves
Neurotrophic factors
Oils & fats
Pollutants
Proteins
Reporter gene
RNA
Skin
Skin diseases
Tryptophan
Ultraviolet radiation
title Aromatic oil from lavender as an atopic dermatitis suppressant
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