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7,3',4'-三羟基异黄酮可改善粉尘螨诱导的 NC/Nga 小鼠特应性皮炎的发展。

7,3',4'-Trihydroxyisoflavone Ameliorates the Development of Dermatophagoides farinae-Induced Atopic Dermatitis in NC/Nga Mice.

机构信息

School of Food Science and Biotechnology, Kyungpook National University, Daegu 702-701, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2013;2013:636597. doi: 10.1155/2013/636597. Epub 2013 Nov 13.

DOI:10.1155/2013/636597
PMID:24324516
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3845246/
Abstract

Atopic dermatitis is an inflammatory and chronically relapsing skin disorder that commonly occurs in children; the number of atopic dermatitis patients is increasing. The cause and mechanism of atopic dermatitis have not been defined clearly, although many studies are ongoing. Epidemiological studies suggest that soybean and its isoflavones have immunoregulatory activities. Here, we report that 7,3',4'-trihydroxyisoflavone (7,3',4'-THIF), a major metabolite of daidzin, effectively inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO), tumor necrosis factor (TNF)- α , and interleukin (IL)-6 production in RAW 264.7 cells, and also reduced β -hexosaminidase secretion in RBL-2H3 cells. Moreover, 7,3',4'-THIF significantly reduced scratching time, transepidermal water loss, and mast cell infiltration. It also decreased protease-activated receptor (PAR)-2 and IL-4 expression and increased filaggrin expression in skin lesions of NC/Nga mice. These results suggest that 7,3',4'-THIF improves Dermatophagoides farina body extract-induced atopic dermatitis in NC/Nga mice.

摘要

特应性皮炎是一种炎症性和慢性复发性皮肤病,常见于儿童;特应性皮炎患者的数量正在增加。尽管正在进行许多研究,但特应性皮炎的病因和发病机制仍未明确。流行病学研究表明,大豆及其异黄酮具有免疫调节活性。在这里,我们报告大豆苷元的主要代谢物 7,3',4'-三羟基异黄酮(7,3',4'-THIF)有效抑制脂多糖(LPS)诱导的 RAW 264.7 细胞中一氧化氮(NO)、肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6的产生,还降低 RBL-2H3 细胞中β-己糖胺酶的分泌。此外,7,3',4'-THIF 显著减少了划痕时间、经表皮水分流失和肥大细胞浸润。它还降低了 NC/Nga 小鼠皮肤病变中蛋白酶激活受体(PAR)-2 和 IL-4 的表达,增加了丝聚蛋白的表达。这些结果表明,7,3',4'-THIF 改善了 NC/Nga 小鼠粉尘螨提取物诱导的特应性皮炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/e062e4c733e9/ECAM2013-636597.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/2a57cc964d8d/ECAM2013-636597.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/b54058840cb4/ECAM2013-636597.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/d3e74ce1b708/ECAM2013-636597.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/fa691a1b969a/ECAM2013-636597.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/e062e4c733e9/ECAM2013-636597.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/2a57cc964d8d/ECAM2013-636597.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/b54058840cb4/ECAM2013-636597.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/d3e74ce1b708/ECAM2013-636597.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/fa691a1b969a/ECAM2013-636597.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e53/3845246/e062e4c733e9/ECAM2013-636597.005.jpg

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