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Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro

Artemisia apiacea Hance is a traditional herbal medicine used for treating eczema and jaundice in Eastern Asia including China, Korea, and Japan. However, the biological and pharmacological actions of Artemisia apiacea Hance in atopic dermatitis (AD) are not fully understood. An ethanolic extract of...

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Autores principales: Yang, Ju-Hye, Lee, Esther, Lee, BoHyoung, Cho, Won-Kyung, Ma, Jin Yeul, Park, Kwang-Il
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073925/
https://www.ncbi.nlm.nih.gov/pubmed/29932162
http://dx.doi.org/10.3390/nu10070806
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author Yang, Ju-Hye
Lee, Esther
Lee, BoHyoung
Cho, Won-Kyung
Ma, Jin Yeul
Park, Kwang-Il
author_facet Yang, Ju-Hye
Lee, Esther
Lee, BoHyoung
Cho, Won-Kyung
Ma, Jin Yeul
Park, Kwang-Il
author_sort Yang, Ju-Hye
collection PubMed
description Artemisia apiacea Hance is a traditional herbal medicine used for treating eczema and jaundice in Eastern Asia including China, Korea, and Japan. However, the biological and pharmacological actions of Artemisia apiacea Hance in atopic dermatitis (AD) are not fully understood. An ethanolic extract of Artemisia apiacea Hance (EAH) was tested in vitro and in vivo to investigate its anti-inflammatory activity and anti-atopic dermatitis effects. The results showed that EAH dose-dependence inhibited production of regulated on activation, normal T-cell expressed and secreted (RANTES), interleukin (IL)-6, IL-8, and thymus and activation-regulated chemokine (TARC). EAH inhibited the activation of p38, extracellular signal-regulated kinases (ERK), and STAT-1 and suppressed the degradation of inhibited both nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha (IκB-α) in TNF-α/IFN-γ–stimulated HaCaT cells. EAH also suppressed the translocation of inflammation transcription factors such as NF-κB p65 in TNF-α/IFN-γ–stimulated HaCaT cells. In addition, EAH reduced 2,4-dinitrochlorobenzene (DNCB)-induced ear thickness and dorsal skin thickness in a dose-dependent manner. EAH appeared to regulate chemokine formation by inhibiting activation of and ERK as well as the NK-κB pathways. Furthermore, EAH significantly improved the skin p38 conditions in a DNCB-induced AD-like mouse model.
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spelling pubmed-60739252018-08-13 Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro Yang, Ju-Hye Lee, Esther Lee, BoHyoung Cho, Won-Kyung Ma, Jin Yeul Park, Kwang-Il Nutrients Article Artemisia apiacea Hance is a traditional herbal medicine used for treating eczema and jaundice in Eastern Asia including China, Korea, and Japan. However, the biological and pharmacological actions of Artemisia apiacea Hance in atopic dermatitis (AD) are not fully understood. An ethanolic extract of Artemisia apiacea Hance (EAH) was tested in vitro and in vivo to investigate its anti-inflammatory activity and anti-atopic dermatitis effects. The results showed that EAH dose-dependence inhibited production of regulated on activation, normal T-cell expressed and secreted (RANTES), interleukin (IL)-6, IL-8, and thymus and activation-regulated chemokine (TARC). EAH inhibited the activation of p38, extracellular signal-regulated kinases (ERK), and STAT-1 and suppressed the degradation of inhibited both nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha (IκB-α) in TNF-α/IFN-γ–stimulated HaCaT cells. EAH also suppressed the translocation of inflammation transcription factors such as NF-κB p65 in TNF-α/IFN-γ–stimulated HaCaT cells. In addition, EAH reduced 2,4-dinitrochlorobenzene (DNCB)-induced ear thickness and dorsal skin thickness in a dose-dependent manner. EAH appeared to regulate chemokine formation by inhibiting activation of and ERK as well as the NK-κB pathways. Furthermore, EAH significantly improved the skin p38 conditions in a DNCB-induced AD-like mouse model. MDPI 2018-06-22 /pmc/articles/PMC6073925/ /pubmed/29932162 http://dx.doi.org/10.3390/nu10070806 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Yang, Ju-Hye
Lee, Esther
Lee, BoHyoung
Cho, Won-Kyung
Ma, Jin Yeul
Park, Kwang-Il
Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro
title Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro
title_full Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro
title_fullStr Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro
title_full_unstemmed Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro
title_short Ethanolic Extracts of Artemisia apiacea Hance Improved Atopic Dermatitis-Like Skin Lesions In Vivo and Suppressed TNF-Alpha/IFN-Gamma–Induced Proinflammatory Chemokine Production In Vitro
title_sort ethanolic extracts of artemisia apiacea hance improved atopic dermatitis-like skin lesions in vivo and suppressed tnf-alpha/ifn-gamma–induced proinflammatory chemokine production in vitro
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073925/
https://www.ncbi.nlm.nih.gov/pubmed/29932162
http://dx.doi.org/10.3390/nu10070806
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