Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model
Guohong Hu, Xiansheng Zhou Dermatology Hospital of Jiangxi Province, Nanchang, 330001, Jiangxi, People’s Republic of ChinaCorrespondence: Guohong HuDermatology Hospital of Jiangxi Province, No. 388 Yingbin North Road, Nanchang, 330001, Jiangxi, People’s Republic of ChinaTel +86-791-85221034Email 200...
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2021
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oai:doaj.org-article:16c0d210e9ab41bf861f9c20e3b8cf752021-11-16T18:47:50ZGallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model1178-7015https://doaj.org/article/16c0d210e9ab41bf861f9c20e3b8cf752021-11-01T00:00:00Zhttps://www.dovepress.com/gallic-acid-ameliorates-atopic-dermatitis-like-skin-inflammation-throu-peer-reviewed-fulltext-article-CCIDhttps://doaj.org/toc/1178-7015Guohong Hu, Xiansheng Zhou Dermatology Hospital of Jiangxi Province, Nanchang, 330001, Jiangxi, People’s Republic of ChinaCorrespondence: Guohong HuDermatology Hospital of Jiangxi Province, No. 388 Yingbin North Road, Nanchang, 330001, Jiangxi, People’s Republic of ChinaTel +86-791-85221034Email 2009020212@st.btbu.edu.cnBackground: Gallic acid (GA) has an anti-inflammatory effect by regulating inflammatory molecules. This study aimed to investigate the effect of GA on atopic dermatitis (AD)-like skin inflammation.Methods: 4-dinitrochlorobenzene (DNCB) was used to induce an AD-like skin inflammation model. The effect of GA on DNCB-induced inflammation was assessed by measuring the thickness and histopathological examination of the ear. Serum IgE and TNF-α levels were detected. The effect of GA on lymph nodes was determined by measuring the weights and mRNA/protein expression levels of TNF-α, IL-4, IFN-γ and IL-17. Ratio of Treg cells and Th17 cells was also analyzed.Results: It was found that the thickness and pathology of the ear were significantly improved by GA in the DNCB-induced mice. Serum IgE and TNF-α levels were significantly reduced in GA-treated model mice compared to the model group. GA treatment lowered the weight of lymph node and the expression of mRNAs of TNF-α, IL-4, IFN-γ, and IL-17 of lymph node. In the ear, inflammatory factors (IL-4, IL-5, IL-17, or IL-23) showed a significant decrease in GA-treated model mice versus model mice, while the expression levels of IL-10 and TGF-β showed a great increase in GA-treated model mice. ROR-γt showed a decrease in GA-treated model group, along with an increase expression of SOCS3.Conclusion: GA could ameliorate AD-like skin inflammation possibly through Th17 mediated immune regulation in a DNCB-induced mouse model.Keywords: 4-dinitrochlorobenzene, DNCB, Th17, IL-10, TGF-β, IFN-γHu GZhou XDove Medical Pressarticle4-dinitrochlorobenzene (dncb)th17il-10tgf-βifn-γDermatologyRL1-803ENClinical, Cosmetic and Investigational Dermatology, Vol Volume 14, Pp 1675-1683 (2021) |
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4-dinitrochlorobenzene (dncb) th17 il-10 tgf-β ifn-γ Dermatology RL1-803 |
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4-dinitrochlorobenzene (dncb) th17 il-10 tgf-β ifn-γ Dermatology RL1-803 Hu G Zhou X Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model |
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Guohong Hu, Xiansheng Zhou Dermatology Hospital of Jiangxi Province, Nanchang, 330001, Jiangxi, People’s Republic of ChinaCorrespondence: Guohong HuDermatology Hospital of Jiangxi Province, No. 388 Yingbin North Road, Nanchang, 330001, Jiangxi, People’s Republic of ChinaTel +86-791-85221034Email 2009020212@st.btbu.edu.cnBackground: Gallic acid (GA) has an anti-inflammatory effect by regulating inflammatory molecules. This study aimed to investigate the effect of GA on atopic dermatitis (AD)-like skin inflammation.Methods: 4-dinitrochlorobenzene (DNCB) was used to induce an AD-like skin inflammation model. The effect of GA on DNCB-induced inflammation was assessed by measuring the thickness and histopathological examination of the ear. Serum IgE and TNF-α levels were detected. The effect of GA on lymph nodes was determined by measuring the weights and mRNA/protein expression levels of TNF-α, IL-4, IFN-γ and IL-17. Ratio of Treg cells and Th17 cells was also analyzed.Results: It was found that the thickness and pathology of the ear were significantly improved by GA in the DNCB-induced mice. Serum IgE and TNF-α levels were significantly reduced in GA-treated model mice compared to the model group. GA treatment lowered the weight of lymph node and the expression of mRNAs of TNF-α, IL-4, IFN-γ, and IL-17 of lymph node. In the ear, inflammatory factors (IL-4, IL-5, IL-17, or IL-23) showed a significant decrease in GA-treated model mice versus model mice, while the expression levels of IL-10 and TGF-β showed a great increase in GA-treated model mice. ROR-γt showed a decrease in GA-treated model group, along with an increase expression of SOCS3.Conclusion: GA could ameliorate AD-like skin inflammation possibly through Th17 mediated immune regulation in a DNCB-induced mouse model.Keywords: 4-dinitrochlorobenzene, DNCB, Th17, IL-10, TGF-β, IFN-γ |
format |
article |
author |
Hu G Zhou X |
author_facet |
Hu G Zhou X |
author_sort |
Hu G |
title |
Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model |
title_short |
Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model |
title_full |
Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model |
title_fullStr |
Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model |
title_full_unstemmed |
Gallic Acid Ameliorates Atopic Dermatitis-Like Skin Inflammation Through Immune Regulation in a Mouse Model |
title_sort |
gallic acid ameliorates atopic dermatitis-like skin inflammation through immune regulation in a mouse model |
publisher |
Dove Medical Press |
publishDate |
2021 |
url |
https://doaj.org/article/16c0d210e9ab41bf861f9c20e3b8cf75 |
work_keys_str_mv |
AT hug gallicacidamelioratesatopicdermatitislikeskininflammationthroughimmuneregulationinamousemodel AT zhoux gallicacidamelioratesatopicdermatitislikeskininflammationthroughimmuneregulationinamousemodel |
_version_ |
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