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Aflatoxins are produced as secondary metabolites by the toxigenic Aspergillus fungi. Among the aflatoxins, aflatoxin B1 (AFB1) is a common contaminant of global concern in human and animal food products. Prolonged exposure to AFB1 may provoke hepatocyte pyroptosis and oxidative stress, which leads to liver damage. Dietary polyphenols could protect the liver from a wide range of toxins. Curcumin, a polyphenolic substance derived from turmeric, is rich in pharmacological activity. The aim of this study was to systematically investigate the protective effects of curcumin against AFB1-induced liver injury in mice and to explore the possible molecular mechanisms. BALB/c mice received oral gavage of AFB1 (0.75 mg/kg) and curcumin (100 or 200 mg/kg) for 30 days. Our data demonstrated that curcumin attenuated AFB1-induced weight loss in mice and rescued liver injury by mitigating the alterations in pathology and liver function with AFB1 exposure. Curcumin reduced the accumulation of AFB1-DNA adducts in the liver and alleviated hepatotoxicity by inhibiting AFB1-induced oxidative stress and potentiating glutathione S-transferase (GST)-mediated phase II detoxification. In addition, curcumin significantly reduced the characteristic indices of AFB1-induced pyroptosis, such as the expression of mRNAs for genes related to NOD-like receptor protein 3 (NLRP3) inflammasome assembly and activation, the expression of key proteins (NLRP3, Caspase-1 and GSDMD). The release of interleukin-1β (IL-1β) and interleukin-18 (IL-18) in the serum detected by ELISA was also significantly decreased. Notably, administration of curcumin upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its related downstream antioxidant molecules (SOD, CAT, HO-1, NQO1) and phase II detoxification enzyme-related molecules (GST, GSH, GSS, GCLC, GCLM) in the presence of AFB1 exposure. To summarize, our results indicated that curcumin could modulate the NLRP3 inflammasome and Nrf2 signaling pathways to attenuate AFB1-induced liver pyroptotic damage and oxidative stress. [ABSTRACT FROM AUTHOR]

Simple Summary: This study clarified for the first time that the Nrf2 and NF-κB signaling pathways in ducks are related to the antioxidant and anti-inflammatory effects. For the first time, we found that dietary resveratrol (RES) effectively alleviated the inflammatory response caused by lipopolysaccharide (LPS) by reducing oxidative stress and endoplasmic reticulum stress, alternating the blood biochemical index, and restoring the destruction of hepatocyte morphology. The results of this study provide strong evidence that dietary RES improved the anti-inflammatory ability and the growth performance of ducks. The aim of this study was to explore the effect of dietary resveratrol on the growth performance and anti-inflammatory mechanism in ducks. A total of 280 one-day-old specific pathogen-free male ducklings (Anas platyrhynchos) with an average body weight of 35 ± 1 g were randomly divided into two dietary treatment groups with different supplementation levels of resveratrol for growth performance experiments: R0 and R400 (0 and, 400 mg kg−1 resveratrol, respectively). At the age of 28 days, 16 ducks were selected from each treatment group and divided into four subgroups for a 2 × 2 factorial pathological experiment: R0; R400; R0 + LPS; R400 + LPS, (0 mg kg−1 resveratrol, 400 mg kg−1 resveratrol, 0 mg kg−1 resveratrol, 400 mg kg−1 resveratrol + 5 mg lipopolysaccharide/kg body weight). The results showed that resveratrol significantly improved final body weight and average daily gain (p < 0.01) and alleviated the lipopolysaccharide-induced inflammatory response with a reduction in IL-1β and IL-6 in the plasma and the liver (p < 0.05). Resveratrol improved mRNA levels of Nrf2 and HO-1 and decreased the mRNA levels of TLR4 and NF-κB in duck liver (p < 0.05). Dietary resveratrol can improve growth performance and reduce inflammation through the Nrf2/HO-1 and TLR4/NF-κB signaling pathways in duck. [ABSTRACT FROM AUTHOR]

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 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. [ABSTRACT FROM AUTHOR]