- 2026-06-10
- Frontiers in medicine 13
- Yanan Zhao
- Zhongyu Wang
- Mengchao Xu
- Meilin Wang
- Fanke Wang
- Hongfei Pang
- Yuhang Liu
- Xintong Li
- Haixiao Li
- Wenya Zhang
- Han Song
- Ruizhe Shi
- Jie Lin
- Zhen Wang
- Yuanyuan Wang
- Haibo Jiang
Study Design
- Type
- Systematic Review
- Sample size
- n = 74
- Population
- 738 animals (from 63 studies) with digestive system diseases
- Methods
- comprehensive literature search and meta-analysis in accordance with PRISMA guidelines
Background
Epigallocatechin-3-gallate (EGCG) constitutes the main component of tea polyphenols found in tea leaves and has been found to have a positive therapeutic effect on various digestive system diseases. However, no systematic review has been conducted on the research progress and mechanisms of EGCG in relation to digestive system diseases, an its toxicity.Methods
We conducted a comprehensive literature search for preclinical studies from the inception of each database to 28th September 2025, including Embase, PubMed, Web of Science, China National Knowledge Infrastructure and Veipu Information. These studies were manually screened based on predefined criteria. A comprehensive literature review and meta-analysis were then performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.Results
A total of 74 animal studies were initially included. Following screening, 63 studies (involving 738 animals) met the inclusion criteria for the meta-analysis. EGCG's animal experiments in digestive system diseases primarily focus on tongue squamous cancer, colorectal cancer, liver cancer, ulcerative colitis, gastric cancer, and functional gastrointestinal disorders. EGCG also has positive effects on pancreatic cancer, radiation enteritis, hepatitis B, oral cancer, esophageal cancer, radiation-induced esophagitis, hepatitis C, acute pancreatitis, fatty liver, and cancer prevention. The potential common pathways include VEGF, EGFR, Notch, Bax/Caspase, Nrf2/UGTIA10, JAK/STAT, NF-κB, IGF/IGF-IR, Caspase-1, HIF-1α/VEGF, TGFβ/p-ERK/p-Smad1/2 and M1/M2 cell polarization. EGCG suppresses cell proliferation through the induction of apoptosis; however, its underlying mechanisms warrant further investigation. Administration of high-dose EGCG alone can induce hepatotoxicity, an effect that is exacerbated under inflammatory conditions. In the context of diabetes, EGCG may also lead to nephrotoxicity. It should be noted that these toxic doses substantially exceed the levels typically attained through normal dietary consumption of tea. The mechanisms responsible for EGCG-mediated toxicity remain to be fully elucidated.Conclusion
In vivo studies have indicated the potential efficacy of EGCG in managing gastrointestinal diseases. However, further investigations are necessary to validate its therapeutic benefits, elucidate the underlying mechanisms, and assess its potential toxicity.