EGCG Alleviates DSS-Induced Colitis by Inhibiting Ferroptosis Through the Activation of the Nrf2-GPX4 Pathway and Enhancing Iron Metabolism

作者：Junzhou Chen, Conghui Yin, Yilong Zhang, Xin Lai, Chen Liu, Yuheng Luo, Junqiu Luo, Jun He, Bing Yu, Quyuan Wang, Huifen Wang, Daiwen Chen, Aimin Wu · 发表于：Nutrients · 年份：2025 · DOI：10.3390/nu17030547 · 被引用次数：20 · 研究领域：Ferroptosis and cancer prognosis、Immune cells in cancer、Inflammasome and immune disorders

BACKGROUND: Ferroptosis is a regulated cell death process linked to various diseases. This study explored whether Epigallocatechin-3-gallate (EGCG), a tea-derived antioxidant, could regulate ferroptosis to alleviate dextran sulfate sodium (DSS)-induced colitis. METHODS: A DSS-induced colitis model was used to assess EGCG's effects. Ferroptosis markers, oxidative stress, and iron metabolism were evaluated, alongside Nrf2-GPX4 pathway activation and ferritin (FTH/L) expression. RESULTS: Iron dysregulation and oxidative stress contributed to DSS-induced colitis by activating ferroptosis in colonic epithelial cells. EGCG supplementation inhibited ferroptosis, reducing oxidative damage. Mechanistically, EGCG activated the Nrf2-GPX4 pathway, enhancing antioxidant defense, and improved iron metabolism by upregulating ferritin expression. CONCLUSIONS: EGCG effectively suppressed DSS-induced ferroptosis and colitis, highlighting its potential as a ferroptosis inhibitor and therapeutic agent.