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

特应性皮炎 炎症 医学 NFKB1型 NF-κB Ping(视频游戏) TLR4型 免疫学 传统医学 化学 生物化学 转录因子 计算机安全 计算机科学 基因
作者
Jing Nie,Xiaoyuan Jiang,Guomi Wang,Yanan Xu,Rui Pan,Wantao Yu,Yuanwen Li,Jingxiao Wang
出处
期刊:Journal of Ethnopharmacology [Elsevier BV]
卷期号:329: 118092-118092 被引量:9
标识
DOI:10.1016/j.jep.2024.118092
摘要

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 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. 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.
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