玉屏风散通过TLR4/MyD88/NF-κB信号通路减轻特应性皮炎小鼠的炎症反应。

Yu-Ping-Feng-San alleviates inflammation in atopic dermatitis mice by TLR4/MyD88/NF-κB pathway.

作者信息

Nie Jing, Jiang Xiaoyuan, Wang Guomi, Xu Yanan, Pan Rui, Yu Wantao, Li Yuanwen, Wang Jingxiao

机构信息

Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China; Third Affiliated Hospital, Beijing University of Chinese Medicine, Beijing, China.

FangShan Hospital, Beijing University of Chinese Medicine, Beijing, China.

出版信息

J Ethnopharmacol. 2024 Jul 15;329:118092. doi: 10.1016/j.jep.2024.118092. Epub 2024 Apr 9.

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

Yu-Ping-Feng-San (YPF) is a traditional Chinese medicine formula that has therapeutic effects on allergic diseases such as allergic rhinitis and asthma. However, its potential efficacy and mechanism in the treatment of atopic dermatitis (AD) has not been extensively illustrated.

AIM OF THE STUDY

The purpose of this study was to investigate the efficacy and possible mechanisms of YPF in AD pathogenesis.

METHODS

Network pharmacology and GEO data mining were adopted to firstly identify the potential mechanisms of YPF on AD. Then DNCB induced-AD murine model was established to test the efficacy of YPF and verify its effects on inflammatory cytokines and NF-κB pathway. In addition, molecular docking was performed to detect the binding affinity of YPF's active components with NF-κB pathway related molecules.

RESULTS

Network pharmacology and human data mining suggested that YPF may act on the NF-κB pathway in AD pathogenesis. With DNCB mice model, we found that YPF significantly improved AD symptoms, reduced SCORAD scores, and alleviated skin tissue inflammation in mice. At the same time, the expression of inflammatory cytokines, TNF-α, sPLA2-IIA and IL-6, was down-regulated. Moreover, YPF suppressed TLR4/MyD88/NF-κB pathway in situ in a dose-dependent manner. Molecular docking further confirmed that seven compounds in YPF had exceptional binding properties with TNF-α, IL-6 and TLR4.

CONCLUSION

YPF may help the recovery of AD by inhibiting the TLR4/MyD88/NF-κB pathway, which provides novel insights for the treatment of AD by YPF.

摘要

民族药理学相关性

玉屏风散(YPF)是一种对过敏性鼻炎和哮喘等过敏性疾病具有治疗作用的中药方剂。然而,其在治疗特应性皮炎(AD)方面的潜在疗效和机制尚未得到广泛阐明。

研究目的

本研究旨在探讨玉屏风散在AD发病机制中的疗效及可能机制。

方法

采用网络药理学和GEO数据挖掘方法首先确定玉屏风散对AD的潜在作用机制。然后建立二硝基氯苯诱导的AD小鼠模型,以测试玉屏风散的疗效,并验证其对炎性细胞因子和NF-κB信号通路的影响。此外,进行分子对接以检测玉屏风散活性成分与NF-κB信号通路相关分子的结合亲和力。

结果

网络药理学和人体数据挖掘表明,玉屏风散可能作用于AD发病机制中的NF-κB信号通路。在二硝基氯苯小鼠模型中,我们发现玉屏风散显著改善了AD症状,降低了SCORAD评分,并减轻了小鼠皮肤组织炎症。同时,炎性细胞因子TNF-α、sPLA2-IIA和IL-6的表达下调。此外,玉屏风散以剂量依赖性方式原位抑制TLR4/MyD88/NF-κB信号通路。分子对接进一步证实,玉屏风散中的七种化合物与TNF-α、IL-6和TLR4具有特殊的结合特性。

结论

玉屏风散可能通过抑制TLR4/MyD88/NF-κB信号通路来促进AD的恢复,这为玉屏风散治疗AD提供了新的见解。

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