<br>玉屏风散通过TLR4/MyD88/NF-κB通路减轻特应性皮炎小鼠炎症,Journal of Ethnopharmacology

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玉屏风散通过TLR4/MyD88/NF-κB通路减轻特应性皮炎小鼠炎症
Journal of Ethnopharmacology ( IF 4.8 ) Pub Date : 2024-04-09 , DOI: 10.1016/j.jep.2024.118092
Jing Nie ₁ , Xiaoyuan Jiang ₂ , Guomi Wang ₃ , Yanan Xu ₄ , Rui Pan ₄ , Wantao Yu ₄ , Yuanwen Li ₅ , Jingxiao Wang ₄

Affiliation

玉屏风散（YPF）是一种中药配方，对过敏性鼻炎、哮喘等过敏性疾病有治疗作用。然而，其治疗特应性皮炎（AD）的潜在功效和机制尚未得到广泛阐明。本研究的目的是探讨YPF在AD发病机制中的功效和可能的机制。采用网络药理学和GEO数据挖掘，首先确定了YPF治疗AD的潜在机制。然后建立DNCB诱导的AD小鼠模型来测试YPF的功效并验证其对炎症细胞因子和NF-κB通路的影响。此外，还进行分子对接，检测YPF活性成分与NF-κB通路相关分子的结合亲和力。网络药理学和人类数据挖掘表明，YPF可能作用于AD发病机制中的NF-κB通路。通过 DNCB 小鼠模型，我们发现 YPF 显着改善小鼠 AD 症状，降低 SCORAD 评分，并减轻小鼠皮肤组织炎症。同时，炎症细胞因子TNF-α、sPLA2-IIA和IL-6的表达下调。此外，YPF 以剂量依赖性方式抑制 TLR4/MyD88/NF-κB 通路。分子对接进一步证实YPF中的7种化合物与TNF-α、IL-6和TLR4具有特殊的结合特性。 YPF可能通过抑制TLR4/MyD88/NF-κB通路来帮助AD的恢复，这为YPF治疗AD提供了新的思路。

"点击查看英文标题和摘要"

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

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. The purpose of this study was to investigate the efficacy and possible mechanisms of YPF in AD pathogenesis. 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. 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 a dose-dependent manner. Molecular docking further confirmed that seven compounds in YPF had exceptional binding properties with TNF-α, IL-6 and TLR4. 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.

更新日期：2024-04-09

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