ArticleJournal of inflammation research2025
Yin-Hua Li-Shi Decoction Alleviated Atopic Dermatitis Through Regulating Th Cells Balance and Restoring Epithelial Barrier.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Multi-omics analysis of transcriptomics and proteomics to provide mechanistic insights into the effects of camellia oil in alleviating xerosis cutis.Biochemistry and biophysics reports · 2026Article
- Yin-Hua Li-Shi Formula Exerts Anti-Atopic Dermatitis Effects Through Luteolin Targeting AKT/MAPK-IL-6/IL-17 Axis.Journal of inflammation research · 2026Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Yin-hua Li-shi Decoction (YLD), a traditional Chinese medicine formulation, has been employed as a complementary therapy for atopic dermatitis (AD). Nevertheless, its precise therapeutic mechanisms remained unexplored. Methods: YLD components were identified by LC-MS, and quality control was performed using HPLC. In vitro, flow cytometry was used to assess YLD toxicity and its effect on inhibiting pro-inflammatory macrophages. In vivo, AD mice model was induced by daily topical MC903 application on mice ears for 15 days. Mice received oral YLD (1.50, 3.00, or 6.00 g/mL) once daily for 14 days. Disease progression was tracked by measuring skin thickness in mice. ELISA, western blot, and immunohistochemistry were used to analyze YLD ability to regulate inflammatory factors and restore skin barrier proteins. Flow cytometry was additionally used to investigate YLD modulatory effects on type I, II, and III adaptive immune responses. Results: YLD could inhibit the differentiation of macrophages into M1 phenotype in vitro. In the AD-like mice, YLD ameliorated epidermal hyperkeratosis and skin lesions, decreased the severity scoring of AD, and suppressed the inflammation of the skin in a dose-dependent manner. Moreover, YLD downregulated pro-inflammatory factors such as IL-4/13, TNF-α, TSLP, and IgE antibodies, restored the expression of barrier proteins in the skin, decreased the infiltration of CD4+ T cells in AD skin, and reestablished the balance of Th1/ Th2/ Th17 cells. Conclusion: YLD alleviated AD by regulating the adaptive immune response through modulation of T cell differentiation and cytokine production, and by restoring skin barrier function. The study revealed the therapeutic mechanism of YLD and provided experimental evidence supporting its application in AD treatment.
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