ArticleJournal of experimental pharmacology2025
Article in Journal of experimental pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atopic dermatitis (AD) is a chronic and recurrent inflammatory skin disease. The disruption of the epidermal barrier and the inflammatory response are the key factors for the occurrence and development of this disease. Objective: To evaluate the ability of AAE to inhibit inflammation and promote skin barrier repair in an AD-like three-dimensional (3D) epidermal equivalent model. Methods: Keratinocytes were treated with three AAE concentrations (0.1%, 0.3%, and 1%) to assess their cytotoxic effects using Cell Counting Kit-8. Methyl-β-cyclodextrin and interleukin (IL)-4, IL-13, and IL-25 were used to induce the AD-like model. The expression of skin structural proteins, inflammatory factors, and histopathological manifestations were compared among AAE-treated AD models, an untreated AD model, and normal control models. Results: Expression of the skin barrier proteins filaggrin ( Conclusion: 1% AAE inhibits inflammation and promotes skin barrier function in an AD-like 3D epidermal equivalent model. AAE which mainly includes Arteannuin B, Chlorogenic Acid, Chrysoplenol D, Scopolin, and Vitexicarpin is identified as the putative targets for AD therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.