EGCG attenuates BPA -induced male reproductive toxicity by regulating the blood-testis barrier by suppressing autophagy via AMPK/AKT/mTOR signaling pathway.

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.