Procyanidin A ₁ and its digestive products alleviate acrylamide-induced IPEC-J2 cell damage through regulating Keap1/Nrf2 pathway

Our previous study has revealed that procyanidin A1 (A1) and its simulated digestive product (D-A1) can alleviate acrylamide (ACR)-induced intestine cell damage. However, the underlying mechanism remains unknown. In this study, we elucidated the molecular for A1 and D-A1 to alleviate ACR-stimulated IPEC-J2 cell damage. ACR slightly activated nuclear factor erythroid 2-related 2 (Nrf2) signaling target genes, but activation could not reduce D-A1 could alleviate ACR-induced damage, effect was abrogated in cells transiently transfected with Nrf2 small interfering RNA (siRNA). Further investigation confirmed that D-A1 interacted with Kelch-like ECH-associated protein 1 (Keap1), which boosted stabilization of Nrf2, subsequently promoted translocation into nucleus, further increased expression antioxidant proteins, thereby inhibiting glutathione (GSH) consumption, maintaining redox balance eventually alleviating ACR-induced Importantly, there was no difference between D-A1 treated groups, indicating A1 can tolerate gastrointestinal digestion and may be a potential compound to limit toxicity ACR.