期刊
CHINESE MEDICINE
卷 17, 期 1, 页码 -出版社
BMC
DOI: 10.1186/s13020-021-00555-7
关键词
CTCMDO; Medicinal substance; Atopic dermatitis; MAPK and NF-kappa B pathways
资金
- National Key Research and Development Program: research on key technologies of the ginseng industry and development of massive health products [2017YFC1702100]
- Science and Technology Development Plan Project of Jilin Province [20180623041TC, 20210401111YY]
- Jilin Province Education Department Project [JJKH20210970KJ]
This study analyzed the active ingredients of CTCMDO and established its fingerprint. It was found that CTCMDO could suppress itch behavior in a dose-dependent manner and improve AD by inhibiting the production of cytokines, reversing the upregulation of itch-related genes, and suppressing the phosphorylation of certain protein kinases.
Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease accompanied with itchy and scaly rash. Compound traditional Chinese medicine dermatitis ointment (CTCMDO) consists of a mixture of extracts from five plants, which had been used in AD treatment due to good anti-inflammatory and anti-allergic effects. Materials and methods: In this study, high-performance liquid chromatography (HPLC) and liquid chromatography/mass spectrometer (LC/MS) were performed to analyze the active ingredients of CTCMDO in detail and to establish its HPLC fingerprint. Furthermore, the anti-inflammatory and antipruritic activities of CTCMDO were studied in the treatment of DNCB-induced AD in mice. Results: A total of 44 compounds including phenylpropionic acid compounds, alkaloid compounds, curcumin compounds and lignans were identified via combined HPLC and LC/MS. A fingerprint with 17 common peaks was established. In AD-like mice, DNCB-induced scratching behavior had been suppressed in the treatment of CTCMDO in a dose-dependent manner. Furthermore, the detailed experimental results indicated that the AD can be effectively improved via inhibiting the production of Th1/2 cytokines in serum, reversing the upregulation of substance P levels of itch-related genes in the skin, and suppressing the phosphorylation of JNK, ERK, and p38 in the skin. Conclusion: This work indicated that CTCMDO can significantly improve AD via attenuating the pathological alterations of Th1/2 cytokines and itch-related mediators, as well as inhibiting the phosphorylation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappa B).
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