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Yu-Ping-Feng-San alleviates inflammation in atopic dermatitis mice by TLR4/MyD88/NF-κB pathway.
Nie, Jing; Jiang, Xiaoyuan; Wang, Guomi; Xu, Yanan; Pan, Rui; Yu, Wantao; Li, Yuanwen; Wang, Jingxiao.
Affiliation
  • Nie J; Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China; Third Affiliated Hospital, Beijing University of Chinese Medicine, Beijing, China. Electronic address: 805051012@qq.com.
  • Jiang X; FangShan Hospital, Beijing University of Chinese Medicine, Beijing, China. Electronic address: jxy_93@163.com.
  • Wang G; Shanghai Skin Disease Hospital, Institute of Dermatology, School of Medicine, Tongji University, Shanghai, China. Electronic address: guomiwang1@163.com.
  • Xu Y; School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. Electronic address: 2992205124@qq.com.
  • Pan R; School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. Electronic address: 434298937@qq.com.
  • Yu W; School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. Electronic address: yuwantao998@163.com.
  • Li Y; Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China. Electronic address: b00485@bucm.edu.cn.
  • Wang J; School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China. Electronic address: 201801022@bucm.edu.cn.
J Ethnopharmacol ; 329: 118092, 2024 Jul 15.
Article in En | MEDLINE | ID: mdl-38604509
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.
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Full text: 1 Database: MEDLINE Main subject: Drugs, Chinese Herbal / Signal Transduction / NF-kappa B / Dermatitis, Atopic / Toll-Like Receptor 4 / Myeloid Differentiation Factor 88 / Molecular Docking Simulation Language: En Journal: J Ethnopharmacol Year: 2024 Type: Article

Full text: 1 Database: MEDLINE Main subject: Drugs, Chinese Herbal / Signal Transduction / NF-kappa B / Dermatitis, Atopic / Toll-Like Receptor 4 / Myeloid Differentiation Factor 88 / Molecular Docking Simulation Language: En Journal: J Ethnopharmacol Year: 2024 Type: Article