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Epigallocatechin-3-gallate inhibits the collagen accumulation of oral submucous fibrosis induced by arecoline

Affiliation
Key Laboratory of Tropical Biological Resources of Ministry of Education and Hainan Engineering Research Center for Drug Screening and Evaluation ,School of Pharmaceutical Sciences ,Hainan University ,Haikou ,China
Gao, Ge;
Affiliation
Key Laboratory of Tropical Biological Resources of Ministry of Education and Hainan Engineering Research Center for Drug Screening and Evaluation ,School of Pharmaceutical Sciences ,Hainan University ,Haikou ,China
Lin, Caipeng;
Affiliation
Key Laboratory of Tropical Biological Resources of Ministry of Education and Hainan Engineering Research Center for Drug Screening and Evaluation ,School of Pharmaceutical Sciences ,Hainan University ,Haikou ,China
Li, Ruibo;
Affiliation
Key Laboratory of Tropical Biological Resources of Ministry of Education and Hainan Engineering Research Center for Drug Screening and Evaluation ,School of Pharmaceutical Sciences ,Hainan University ,Haikou ,China
Xie, Xi;
Affiliation
Key Laboratory of Tropical Biological Resources of Ministry of Education and Hainan Engineering Research Center for Drug Screening and Evaluation ,School of Pharmaceutical Sciences ,Hainan University ,Haikou ,China
Luo, Hai-Bin

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 in vitro and in vivo . 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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License Holder: Copyright © 2025 Gao, Lin, Li, Xie and Luo.

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