Wang Qingyan, Su Yunjie, Yang Qian, Beta Trust, Shen Fei, Liu Qin
College of Food Science and Engineering, Nanjing University of Finance and Economics, Collaborative Innovation Center for Modern Grain Circulation and Safety, Nanjing 210023, China.
College of Food Science and Engineering, Nanjing University of Finance and Economics, Collaborative Innovation Center for Modern Grain Circulation and Safety, Nanjing 210023, China.
Comp Biochem Physiol C Toxicol Pharmacol. 2025 Nov;297:110298. doi: 10.1016/j.cbpc.2025.110298. Epub 2025 Jul 22.
Bisphenol A (BPA) is a typical endocrine disrupting chemical widely distributed in the environment and in food systems. The adverse effects of BPA on reproductive health have posed major concerns worldwide. The aim of this study was to determine the potential of epigallocatechin gallate (EGCG) to protect against BPA-induced male reproductive toxicity and investigate the underlying protective mechanism. The protective effects of EGCG on BPA-induced reproductive toxicity were investigated using male zebrafish model. The results showed that EGCG alleviated BPA-induced developmental toxicity of F1 generation of zebrafish, reversed testis disorder and combated the blood-testis barrier (BTB) damage caused by BPA in zebrafish. In order to unravel the underlying mechanism, TM4 cell - constructed BTB model was used for further study. The results indicated that EGCG counteracted the damage induced by BPA on the integrity of BTB model and reduced the autophagy caused by BPA. Furthermore, EGCG effectively inhibited the BPA-induced upregulation of the expression level of AMPK (p-AMPKα/AMPKα), significantly restored the BPA-mediated downregulation of the expression levels of p-mTOR/mTOR, p-AKT/AKT and Raptor. The results suggested that EGCG mitigated the BPA-induced male reproductive toxicity through maintaining the integrity of BTB by inhibiting the autophagy mediated by AMPK/AKT/mTOR signaling pathway. This study provided a strategy for combating the BPA-induced reproductive toxicity using a well-known bioactive component as a potential therapeutic approach.
双酚A（BPA）是一种典型的内分泌干扰化学物质，广泛分布于环境和食品体系中。BPA对生殖健康的不利影响已引起全球主要关注。本研究的目的是确定表没食子儿茶素没食子酸酯（EGCG）预防BPA诱导的雄性生殖毒性的潜力，并探究其潜在的保护机制。使用雄性斑马鱼模型研究了EGCG对BPA诱导的生殖毒性的保护作用。结果表明，EGCG减轻了BPA诱导的斑马鱼F1代发育毒性，逆转了睾丸紊乱，并对抗了BPA对斑马鱼血睾屏障（BTB）的损伤。为了阐明潜在机制，使用TM4细胞构建的BTB模型进行进一步研究。结果表明，EGCG抵消了BPA对BTB模型完整性的损伤，并减少了BPA引起的自噬。此外，EGCG有效抑制了BPA诱导的AMPK（p-AMPKα/AMPKα）表达水平上调，显著恢复了BPA介导的p-mTOR/mTOR、p-AKT/AKT和Raptor表达水平下调。结果表明，EGCG通过抑制AMPK/AKT/mTOR信号通路介导的自噬来维持BTB的完整性，从而减轻BPA诱导的雄性生殖毒性。本研究提供了一种策略，即使用一种知名的生物活性成分作为潜在的治疗方法来对抗BPA诱导的生殖毒性。
