ArticleFrontiers in pharmacology2026
Article in Frontiers in pharmacology, 2026. 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder characterized by pruritus and xerosis. Current treatments for AD primarily involve glucocorticoids and immunosuppressive agents. However, long-term administration of these treatments may lead to significant adverse effects. Therefore, there is an urgent need for effective therapeutic alternatives with improved safety profiles. Purpose: This study investigated the effects of Methods: We analyzed the chemical composition of PNE using high-performance liquid chromatography (HPLC). The anti-AD effects of PNE were evaluated in both an AD-like mouse model induced by calcipotriol (MC903) and a human keratinocyte (HaCaT) cell model stimulated with tumor necrosis factor-alpha and interferon-gamma (TNF-α/IFN-γ). Furthermore, metabolomics analysis of mouse skin tissue was conducted to elucidate the underlying metabolic mechanisms. To investigate the associated signaling pathways, quantitative real-time PCR (qPCR) and Western blotting were performed. Results: In MC903-induced mice, PNE exhibited potent anti-AD effects, including attenuation of AD-like skin lesions and suppression of Th2 cytokines ( Conclusion: PNE exerts anti-AD effects by attenuating Th2-mediated inflammatory responses via modulation of the cGAS-STING pathway. These findings suggest that PNE has the potential to serve as a natural therapeutic option for AD.
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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.