表没食子儿没食子酸酯通过激活Nrf2-GPX4途径抑制铁死亡并增强铁代谢来减轻右旋糖酐硫酸钠诱导的结肠炎。
EGCG Alleviates DSS-Induced Colitis by Inhibiting Ferroptosis Through the Activation of the Nrf2-GPX4 Pathway and Enhancing Iron Metabolism.
作者信息
Chen Junzhou, Yin Conghui, Zhang Yilong, Lai Xin, Liu Chen, Luo Yuheng, Luo Junqiu, He Jun, Yu Bing, Wang Quyuan, Wang Huifen, Chen Daiwen, Wu Aimin
机构信息
Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu 611130, China.
Key Laboratory for Animal Disease-Resistance Nutrition, China Ministry of Education, Sichuan Agricultural University, Chengdu 611130, China.
出版信息
Nutrients. 2025 Jan 31;17(3):547. doi: 10.3390/nu17030547.
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.
背景
铁死亡是一种与多种疾病相关的程序性细胞死亡过程。本研究探讨了茶叶来源的抗氧化剂表没食子儿没食子酸酯（EGCG）是否可以调节铁死亡以减轻葡聚糖硫酸钠（DSS）诱导的结肠炎。
方法
采用DSS诱导的结肠炎模型来评估EGCG的作用。评估了铁死亡标志物、氧化应激和铁代谢，以及Nrf2-GPX4途径的激活和铁蛋白（FTH/L）的表达。
结果
铁调节异常和氧化应激通过激活结肠上皮细胞中的铁死亡导致DSS诱导的结肠炎。补充EGCG可抑制铁死亡，减少氧化损伤。机制上，EGCG激活Nrf2-GPX4途径，增强抗氧化防御，并通过上调铁蛋白表达改善铁代谢。
结论
EGCG有效抑制DSS诱导的铁死亡和结肠炎，突出了其作为铁死亡抑制剂和治疗剂的潜力。
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