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Simple Summary Aflatoxin B1 is ubiquitous in food and feed, which not only poses a great threat to animals, but also affects human health. It is unclear whether resveratrol can resist aflatoxin B1 damage in ducks’ livers. Therefore, the effect of resveratrol supplementation in the diets on liver injury aflatoxin B1was investigated through the gavage of aflatoxin B1. It was found that a diet that includes resveratrol can effectively protect ducks’ livers from acute injury caused by aflatoxin B1. Our study suggests that resveratrol serves as a potential phytochemical feed additive for the treatment of acute aflatoxin B1 poisoning in ducks Abstract The presence of aflatoxin B1 (AFB1) in feed is a serious threat to livestock and poultry health and to human food safety. Resveratrol (Res) is a polyphenolic compound with antioxidant, anti-apoptotic and other biological activities; however, it is not clear whether it can improve AFB1 induced hepatotoxicity. Therefore, this study was conducted to investigate the effects of dietary Res on liver injury induced by AFB1 and its mechanisms. A total of 270 one-day-old male specific pathogen free (SPF) ducks, with no significant difference in weight, were randomly assigned to three groups: the control group, the AFB1 group and the AFB1 + Res group, which were fed a basic diet, a basic diet and a basic diet containing 500 mg/kg Res, respectively. On the 70th day, the ducks in theAFB1 group and the AFB1+ 500 mg/kg Res group were given 60 μg/kg AFB1 via gavage. When comparing the AFB1 group and the AFB1 + Res group and also with the control group, AFB1 significantly increased liver damage, cytochrome P450 (CYP450) and AFB1-DNA adduct content, increased oxidative stress levels and induced liver apoptosis, which was improved by Res supplementation. In sum, the addition of Res to feed can increase the activity of the II-phase enzyme, activate the nuclear factor E2-related factor 2 (Nrf2) signal pathway, and protect ducks’ livers from the toxicity, oxidative stress and inflammatory reaction induced by AFB1.