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

被引:4
作者
Nie, Jing [1 ,2 ]
Jiang, Xiaoyuan [3 ]
Wang, Guomi [4 ]
Xu, Yanan [5 ]
Pan, Rui [5 ]
Yu, Wantao [5 ]
Li, Yuanwen [1 ]
Wang, Jingxiao [5 ]
机构
[1] Beijing Univ Chinese Med, Dongfang Hosp, Beijing, Peoples R China
[2] Beijing Univ Chinese Med, Affiliated Hosp 3, Beijing, Peoples R China
[3] Beijing Univ Chinese Med, FangShan Hosp, Beijing, Peoples R China
[4] Tongji Univ, Shanghai Skin Dis Hosp, Inst Dermatol, Sch Med, Shanghai, Peoples R China
[5] Beijing Univ Chinese Med, Sch Life Sci, Yangguang South St, Beijing 102488, Peoples R China
基金
中国国家自然科学基金;
关键词
Traditional Chinese medicine; Atopic dermatitis; Yu-Ping-Feng-San; NF-kappa B pathway; Inflammation; NF-KAPPA-B; ALLERGIC INFLAMMATION; YUPINGFENG GRANULES; TNF-ALPHA; BARRIER;
D O I
10.1016/j.jep.2024.118092
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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-kappa B pathway. In addition, molecular docking was performed to detect the binding affinity of YPF's active components with NF-kappa B pathway related molecules. Results: Network pharmacology and human data mining suggested that YPF may act on the NF-kappa B 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-alpha, sPLA2-IIA and IL-6, was down-regulated. Moreover, YPF suppressed TLR4/MyD88/NF kappa B pathway in situ in a dose-dependent manner. Molecular docking further confirmed that seven compounds in YPF had exceptional binding properties with TNF-alpha, IL-6 and TLR4. Conclusion: YPF may help the recovery of AD by inhibiting the TLR4/MyD88/NF-kappa B pathway, which provides novel insights for the treatment of AD by YPF.
引用
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页数:13
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