摘要Our previous study has demonstrated that procyanidin A1(A1)and its simulated digestive product(D-A1)can prevent acrylamide(ACR)-induced cytotoxicity in small intestine cells.However,the potential mechanism remains poorly understood.In this study,ACR treatment was found to increase the levels of 8-hydroxy-deoxyguanine(8-OHdG)and phosphorated histone H2AX(γH2AX),two DNA damage markers,thereby resulting in cell cycle arrest in the G2/M phase;whereas both A1 and D-A1 could prevent the phosphorylation of ataxia telangiectasia mutated(ATM)and checkpoint kinase 2(Chk2),and then regulate the expression of G2/M phase-related proteins,finally maintaining normal cell cycle progression.Moreover,A1 and D-A1 could increase the B cell lymphoma 2(Bcl-2)/Bcl2-associated X(Bax)ratio and decrease the expression of cleaved caspase-3 and cleaved caspase-9 proteins to alleviate ACR-induced cell apoptosis,which might be related to the inhibition of the mitogen-activated protein kinase(MAPK)pathway.More importantly,A1 showed no remarkable variation in inhibitory effect before and after digestion,indicating that it can endure gastrointestinal digestion and may be a promising phytochemical to alleviate ACR-induced intestinal cell damage.