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Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model
BACKGROUND: Recent studies have reported that glucosamine (GlcN) showed therapeutic effects in allergic diseases such as asthma and rhinitis, and its mechanisms include the suppression of T helper type 2 immune responses and the nuclear factor-κB pathway. OBJECTIVE: We aimed to investigate the effec...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Dermatological Association; The Korean Society for Investigative Dermatology
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7992559/ https://www.ncbi.nlm.nih.gov/pubmed/33911646 http://dx.doi.org/10.5021/ad.2019.31.5.538 |
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author | Yoon, Hee Seong Byun, Ji Won Shin, Jeonghyun Kim, Young Hyo Choi, Gwang Seong |
author_facet | Yoon, Hee Seong Byun, Ji Won Shin, Jeonghyun Kim, Young Hyo Choi, Gwang Seong |
author_sort | Yoon, Hee Seong |
collection | PubMed |
description | BACKGROUND: Recent studies have reported that glucosamine (GlcN) showed therapeutic effects in allergic diseases such as asthma and rhinitis, and its mechanisms include the suppression of T helper type 2 immune responses and the nuclear factor-κB pathway. OBJECTIVE: We aimed to investigate the effect of GlcN on atopic dermatitis (AD) in an animal model. METHODS: Twenty-five BALB/c mice were divided into five groups (groups A~E). Group A was the phosphate-buffered saline (PBS)-treated group without AD induction. Group B was the PBS control group with AD induction. Groups C to E were the AD induction groups, which were treated with three different doses of GlcN (10 mg, 20 mg, and 40 mg, respectively). Histopathological examination was performed after GlcN administration. Interleukin (IL)-4, IL-13, and IL-17 cytokine levels were measured by enzyme-linked immunosorbent assay using skin biopsy specimens. Serum total immunoglobulin E (IgE) concentrations were measured before and after administration with GlcN or PBS. RESULTS: Clinical dermatitis scores decreased with increasing GlcN dose (p<0.001). Concentrations of tissue IL-13 and IL-17 decreased after GlcN administration (each group: p=0.002 and p<0.001, respectively), but the concentrations of tissue IL-4 did not show differences across groups. Serum IgE levels tended to be lower after GlcN administration (p=0.004). Histopathological scores were not significantly different among groups B~E (p=0.394). CONCLUSION: GlcN improved AD symptoms and decreased tissue IL-13, IL-17, and serum total IgE levels in an animal model. |
format | Online Article Text |
id | pubmed-7992559 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | The Korean Dermatological Association; The Korean Society for Investigative Dermatology |
record_format | MEDLINE/PubMed |
spelling | pubmed-79925592021-04-27 Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model Yoon, Hee Seong Byun, Ji Won Shin, Jeonghyun Kim, Young Hyo Choi, Gwang Seong Ann Dermatol Original Article BACKGROUND: Recent studies have reported that glucosamine (GlcN) showed therapeutic effects in allergic diseases such as asthma and rhinitis, and its mechanisms include the suppression of T helper type 2 immune responses and the nuclear factor-κB pathway. OBJECTIVE: We aimed to investigate the effect of GlcN on atopic dermatitis (AD) in an animal model. METHODS: Twenty-five BALB/c mice were divided into five groups (groups A~E). Group A was the phosphate-buffered saline (PBS)-treated group without AD induction. Group B was the PBS control group with AD induction. Groups C to E were the AD induction groups, which were treated with three different doses of GlcN (10 mg, 20 mg, and 40 mg, respectively). Histopathological examination was performed after GlcN administration. Interleukin (IL)-4, IL-13, and IL-17 cytokine levels were measured by enzyme-linked immunosorbent assay using skin biopsy specimens. Serum total immunoglobulin E (IgE) concentrations were measured before and after administration with GlcN or PBS. RESULTS: Clinical dermatitis scores decreased with increasing GlcN dose (p<0.001). Concentrations of tissue IL-13 and IL-17 decreased after GlcN administration (each group: p=0.002 and p<0.001, respectively), but the concentrations of tissue IL-4 did not show differences across groups. Serum IgE levels tended to be lower after GlcN administration (p=0.004). Histopathological scores were not significantly different among groups B~E (p=0.394). CONCLUSION: GlcN improved AD symptoms and decreased tissue IL-13, IL-17, and serum total IgE levels in an animal model. The Korean Dermatological Association; The Korean Society for Investigative Dermatology 2019-10 2019-08-30 /pmc/articles/PMC7992559/ /pubmed/33911646 http://dx.doi.org/10.5021/ad.2019.31.5.538 Text en Copyright © 2019 The Korean Dermatological Association and The Korean Society for Investigative Dermatology http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Yoon, Hee Seong Byun, Ji Won Shin, Jeonghyun Kim, Young Hyo Choi, Gwang Seong Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model |
title | Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model |
title_full | Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model |
title_fullStr | Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model |
title_full_unstemmed | Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model |
title_short | Therapeutic Effect of Glucosamine on an Atopic Dermatitis Animal Model |
title_sort | therapeutic effect of glucosamine on an atopic dermatitis animal model |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7992559/ https://www.ncbi.nlm.nih.gov/pubmed/33911646 http://dx.doi.org/10.5021/ad.2019.31.5.538 |
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