ArticleCurrent medicinal chemistry2025
Nepetin Attenuates Atopic Dermatitis in HaCaT Cells and BALB/c Mice through MyD88-MKK3/6-Akt Signaling.
Article in Current medicinal chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 3 citations in OpenAlex.
- Flavonoids in atopic dermatitis: mechanisms, delivery innovations, and translational strategies.Frontiers in pharmacology · 2025Review
- Flavonoids: a natural remedy in the prevention and management of diverse diseases.Frontiers in medicine · 2025Review
- Elucidation of Anti-Obesity Mechanisms of Phenolics inLife (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
introductionNepetin is a type of O-methylated flavone (6-hydroxy luteolin) and has been found in many herbal medicines that exhibit various pharmacological properties, including anti-inflammatory responses. Here, we aimed to investigate the efficacy of nepetin in attenuating inflammatory responses in cultured keratinocytes and 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD) in BALB/c mice.
methodsVarious assay methods including cell viability, flow cytometry, fluorometry, confocal microscopy, western blot, ELISA techniques, staining methods, score and scratch frequency assessment, etc. were employed to explore the mechanisms.
resultsLPS-treated keratinocytes showed a significant increase in inflammatory mediators (i- NOS, COX-2, PGES2, and NO) and cytokines (IL-1β, IL-6, and TNF-α) in a dose-dependent manner. Treatment with nepetin prevented LPS-induced cell death and inhibited inflammatory mediators and the production of cytokines in cultured keratinocytes. This inhibition was achieved by nepetin, which inhibited LPS-induced ROS production and the translocation of NF-κB in the cultures, thereby inhibiting the generation of inflammatory mediators and/or cytokines. In a mouse model of AD, treatment with nepetin reduced skin inflammation symptoms in a dose-dependent manner, as evidenced by the significant reduction of inflammation-related cytokines, skin lesions, and behavior scores.
conclusionBased on the present
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Registered trials
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