LAUSR

AIM Acrylamide (AA) is a common heat-generated toxicant in some food. Inhibiting its formation with natural antioxidants is of great significance. The current study aims to investigate the alleviative effect and the underlying mechanism of allicin against AA-induced oxidative stress in BRL-3A cells. MAIN METHODS BRL-3A cells were pretreated with allicin at different concentrations for 2 h, followed by AA treatment. Cell viability was determined by Cell Counting kit-8 (CCK-8). Intracellular reactive oxygen species (ROS) status was measured using the 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) method. Levels of oxidative stress markers were determined by measuring total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and 8-hydroxy-desoxyguanosine (8-OHdG) using commercial kits. Expression of the mitogen-activated protein kinase (MAPK) pathway-related proteins was determined by Western blotting. KEY FINDINGS Allicin markedly mitigated oxidative and DNA damage by increasing the activities of SOD and GSH-Px and decreasing the levels of ROS and 8-OHdG. Concomitant with these biochemical parameters, pretreatment with allicin reversed the impact of AA on the expression of p-JNK, p-ERK1/2 and p-p38. Allicin combined with SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor) enhanced cell viability in the presence of AA, as opposed to SCH772984 (ERK inhibitor). Notably, allicin ameliorated the expression of KGF, Gadd45a, c-Fos, Dusp5 and Phospholipase A2, which were related to liver injury. SIGNIFICANCE Collectively, these findings demonstrate that allicin exerts protective effects against AA-induced oxidative stress by modulating the MAPK signaling pathway in BRL-3A cells.