Frontiers in pharmacology · 2025
Epigallocatechin-3-gallate inhibits the collagen accumulation of oral submucous fibrosis induced by arecoline.
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Gao Ge, Lin Caipeng, Li Ruibo, Xie Xi, Luo Hai-Bin
Аннотация
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.
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.