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岩藻黄质通过调节角质形成细胞和调节性固有淋巴细胞改善特应性皮炎症状。

Fucoxanthin Ameliorates Atopic Dermatitis Symptoms by Regulating Keratinocytes and Regulatory Innate Lymphoid Cells.

机构信息

Molecular Toxicology Lab., Ritsumeikan University, Shiga 525-8577, Japan.

Laboratory of Veterinary Pharmacology, Division of Veterinary Science, Osaka Prefecture University, Graduate School of Life and Environmental Science, Izumisano, Osaka 598-8531, Japan.

出版信息

Int J Mol Sci. 2020 Mar 22;21(6):2180. doi: 10.3390/ijms21062180.

DOI:10.3390/ijms21062180
PMID:32235696
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7139773/
Abstract

Fucoxanthin (FX) is a xanthophyll that is contained abundantly in marine plants. The biological action of FX includes its antioxidant and anti-lipogenic activities, while the precise action of its mechanisms on skin cells has not yet been clarified. The current study examined the effect of FX in comparison with tacrolimus (TAC) on NC/Nga mice, which are an atopic dermatitis (AD) model. FX topical treatment dramatically ameliorated itching behavior over the TAC treatment, which was insufficient for improvement of AD symptoms. In Nc/Nga mice, FX or TAC applied to the skin inhibited eosinophil infiltration with decreased expression of Il-33. FX also stimulated Il-2, Il-5, Il-13, Il-10, and TGF-β expression levels, and Sca1Il-10TGF-β regulatory innate lymphoid cells (ILCreg) were dominantly observed in FX treated skin epidermal keratinocytes and dermal layers. This combined evidence demonstrated that FX exerts anti-inflammatory effects on keratinocytes and ameliorates AD symptoms by regulating ILCreg to normalize immune responses in an atopic dermatitis model.

摘要

褐藻黄素 (FX) 是一种叶黄素，在海洋植物中含量丰富。FX 的生物学作用包括其抗氧化和抗脂肪生成活性，但其对皮肤细胞的确切作用机制尚未阐明。本研究比较了 FX 与他克莫司 (TAC) 对 NC/Nga 小鼠（特应性皮炎 (AD) 模型）的作用。FX 局部治疗可显著改善瘙痒行为，而 TAC 治疗不足以改善 AD 症状。在 Nc/Nga 小鼠中，FX 或 TAC 应用于皮肤可抑制嗜酸性粒细胞浸润，并降低 Il-33 的表达。FX 还刺激 Il-2、Il-5、Il-13、Il-10 和 TGF-β 的表达水平，并且在 FX 处理的皮肤表皮角质形成细胞和真皮层中主要观察到 Sca1Il-10TGF-β 调节性先天淋巴细胞 (ILCreg)。这些综合证据表明，FX 对角质形成细胞发挥抗炎作用，并通过调节 ILCreg 来改善 AD 症状，使特应性皮炎模型中的免疫反应正常化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/7139773/5d2b005fa07d/ijms-21-02180-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/7139773/54b5e80b5b62/ijms-21-02180-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/7139773/3f0b6624f6a1/ijms-21-02180-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/7139773/5d2b005fa07d/ijms-21-02180-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/7139773/54b5e80b5b62/ijms-21-02180-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/7139773/3f0b6624f6a1/ijms-21-02180-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9544/7139773/5d2b005fa07d/ijms-21-02180-g003.jpg

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