ArticleFrontiers in pharmacology2025
Epigallocatechin-3-gallate inhibits the collagen accumulation of oral submucous fibrosis induced by arecoline.
Article in Frontiers in pharmacology, 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.
- A Multifunctional Nucleic Acid Nanomedicine Coregulates Angiogenesis and Fibrosis to Treat Oral Submucous Fibrosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- An organoid-guided roadmap for precision delivery of epigallocatechin gallate in oral submucous fibrosis.Frontiers in bioengineering and biotechnology · 2026Review
- Oral submucosal fibrosis: a comprehensive review on pathogenesis, diagnosis, therapeutics and computational advances.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Oral submucous fibrosis (OSF) is a chronic oral mucosal disease, which exerts a profound impact on patients' daily life and currently lacks efficacious therapeutic interventions. Epigallocatechin-3-gallate (EGCG), the abundant polyphenol found in green tea, exhibits remarkable anti-fibrotic effects on the skin. However, the research on OSF regarding EGCG is relatively limited. Purpose: We aimed to investigate the potential therapeutic effect of EGCG against OSF using an arecoline (ARE) -induced rat model and primary rat oral fibroblasts. Methods: Primary rat oral mucosal fibroblasts (ROMF) were isolated and identified. Optimal ARE concentrations were established using the Cell Counting Kit-8. The impact of ARE on extracellular matrix (ECM)-related protein expression was assessed through RT-qPCR and Western blot techniques. Similarly, the effects of EGCG on ARE-induced ECM changes in ROMF were evaluated. The study also established an OSF model in Sprague-Dawley rats, induced by ARE, with pathological changes characterized using HE and Masson's staining, further assessing the impact of ARE on ECM-related protein expression in rat oral tissues through RT-qPCR and Western blot methods. Results: EGCG effectively suppressed the ARE-induced ECM components while concurrently improving the OSF pathological process Conclusion: The results indicate that the natural product EGCG effectively suppressed the increased ECM components induced by ARE and concurrently improved the OSF pathological process, indicating that EGCG could be potentially a novel anti-fibrotic candidate drug for the treatment of OSF.
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