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褪黑素对人皮肤重建模型中银屑病表型的影响。

Effect of Melatonin on Psoriatic Phenotype in Human Reconstructed Skin Model.

作者信息

Scuderi Sarah Adriana, Cucinotta Laura, Filippone Alessia, Lanza Marika, Campolo Michela, Paterniti Irene, Esposito Emanuela

机构信息

Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D'Alcontres, 31-98166 Messina, Italy.

出版信息

Biomedicines. 2022 Mar 23;10(4):752. doi: 10.3390/biomedicines10040752.

DOI:10.3390/biomedicines10040752
PMID:35453501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9032986/
Abstract

Psoriasis is an inflammatory and auto-immune skin-disease characterized by uncontrolled keratinocyte proliferation. Its pathogenesis is not still fully understood; however, an aberrant and excessive inflammatory and immune response can contribute to its progression. Recently, more attention has been given to the anti-inflammatory and immunomodulators effects of melatonin in inflammatory diseases. The aim of this paper was to investigate the effect of melatonin on psoriatic phenotype and also in infection-associated psoriasis, with an in vitro model using Skinethic Reconstructed Human Epidermis (RHE). An in vitro model was constructed using the RHE, a three-dimensional-model obtained from human primary-keratinocytes. RHE-cells were exposed to a mix of pro-inflammatory cytokines, to induce a psoriatic phenotype; cells were also infected with to aggravate psoriasis disease, and then were treated with melatonin at the concentrations of 1 nM, 10 nM, and 50 nM. Our results demonstrated that melatonin at higher concentrations significantly reduced histological damage, compared to the cytokine and groups. Additionally, the treatment with melatonin restored tight-junction expression and reduced pro-inflammatory cytokine levels, such as interleukin-1β and interleukin-12. Our results suggest that melatonin could be considered a promising strategy for psoriasis-like skin inflammation, as well as complications of psoriasis, such as infection.

摘要

银屑病是一种炎症性自身免疫性皮肤病,其特征为角质形成细胞增殖失控。其发病机制尚未完全明确;然而,异常且过度的炎症和免疫反应会促使其病情进展。近来,褪黑素在炎症性疾病中的抗炎和免疫调节作用受到了更多关注。本文旨在利用Skinethic重组人皮表皮(RHE)体外模型,研究褪黑素对银屑病表型以及感染相关性银屑病的影响。使用从人原代角质形成细胞获得的三维模型RHE构建体外模型。将RHE细胞暴露于促炎细胞因子混合物中以诱导银屑病表型;细胞还用 感染以加重银屑病病情,然后用浓度为1 nM、10 nM和50 nM的褪黑素进行处理。我们的结果表明,与细胞因子和 组相比,较高浓度的褪黑素显著减少了组织学损伤。此外,褪黑素处理可恢复紧密连接表达并降低促炎细胞因子水平,如白细胞介素-1β和白细胞介素-12。我们的结果表明,褪黑素可被视为治疗银屑病样皮肤炎症以及银屑病并发症(如 感染)的一种有前景的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/f23c8d3a5d45/biomedicines-10-00752-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/191eef7857b8/biomedicines-10-00752-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/cf0820ba9f7b/biomedicines-10-00752-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/fa63b8d2b67d/biomedicines-10-00752-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/0210a823d13c/biomedicines-10-00752-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/e649d154dedf/biomedicines-10-00752-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/a49debbb8612/biomedicines-10-00752-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/effc759dbeb2/biomedicines-10-00752-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/f0cba3879b74/biomedicines-10-00752-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/f23c8d3a5d45/biomedicines-10-00752-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/191eef7857b8/biomedicines-10-00752-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/cf0820ba9f7b/biomedicines-10-00752-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/fa63b8d2b67d/biomedicines-10-00752-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/0210a823d13c/biomedicines-10-00752-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/e649d154dedf/biomedicines-10-00752-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/a49debbb8612/biomedicines-10-00752-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/effc759dbeb2/biomedicines-10-00752-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/f0cba3879b74/biomedicines-10-00752-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c7de/9032986/f23c8d3a5d45/biomedicines-10-00752-g009.jpg

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