Exploring EGCG's role in protecting against acetaminophen-induced liver injury

Announcing a new publication for Acta Materia Medica journal. Excessive consumption of acetaminophen (APAP) has emerged as the primary culprit behind drug-induced liver injury (DILI), with N-acetylcysteine serving as the principal antidote.

However, use of N-acetylcysteine is limited to the early stages of APAP-induced DILI and may cause adverse side effects. Consequently, it is imperative to explore alternative therapeutic approaches to alleviate APAP-induced liver toxicity. In this study the mechanisms underlying the protective role of epigallocatechin gallate (EGCG) in DILI were determined.

The authors of this article show that EGCG inhibited NEDD8, thus stabilizing HUWE1, a crucial E3 ubiquitin ligase involved in protein degradation. HUWE1 binds and degrades TFR1, a protein essential for cellular iron uptake and inhibits ferroptosis. By stabilizing HUWE1 and degrading TFR1, EGCG suppressed ferroptosis and ameliorated APAP-induced liver injury. The results highlight the therapeutic potential of EGCG in mitigating DILI through regulation of HUWE1 and ferroptosis, which offers a promising approach for the treatment of DILI.0087.