ArticleNaunyn-Schmiedeberg's archives of pharmacology2024
Fraxin alleviates oral lichen planus by suppressing OCT3-mediated activation of FGF2/NF-κB pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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Who cites it
2 citing papers in PubMed.
- GLP-1 Mitigated Inflammation and Oxidative Stress in Oral Lichen Planus Via JAK-STAT3 Pathway.Biochemical genetics · 2026Article
- Etiopathogenesis of Oral Lichen Planus: A Review.Head and neck pathology · 2025Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral lichen planus (OLP) is a carcinogenic chronic inflammatory oral disease, which lacks effective treatments. Fraxin is an active ingredient of the traditional Chinese medicine Qin Pi, which has an anti-inflammatory effect, but its effect on OLP is unclear. The aim of this study was to investigate the therapeutic effect of fraxin on OLP and the underlying mechanism. Human immortalized keratinocytes (HaCat) were incubated with fraxin (10, 20, or 40 µM) for 48 h and then treated with 10 µg/mL LPS for 24 h. Cell viability and apoptosis were detected. Next, the interaction between OCT3 and FGF2 was predicted by online database and verified by Co-IP analysis. Fraxin, Ad-OCT3, sh-OCT3, and sh-FGF2 were, respectively, applied to treat LPS-incubated HaCat cells, and cell viability, apoptosis, and secretion of inflammatory factors were detected with MTT, flow cytometry, and ELISA assays. Then, the involvement of OCT3 and FGF2 in the prevention of fraxin on HaCat cells from LPS-induced cell apoptosis and inflammation was investigated through multiple rescue experiments. In addition, OLP models were constructed in VDR
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