Mitigation of Aflatoxin B Hepatoxicity by Dietary Is Associated with Activation of NRF2/ARE Signaling in Chicks.

The objective of this study was to explore the mechanism of (HD) in mediating the detoxification of aflatoxin B (AFB)-induced hepatic injury in chicks. A total of 144 one-day-old male broilers (Cobb 500) were randomly assigned to four treatment groups ( = 6 cages/diet, 6 chicks/cage). After three days of acclimation, the broilers were fed either a control diet (Control), Control plus 0.5 mg/kg of AFB, or Control plus 0.5 mg/kg AFB with 500 or 1000 mg/kg HD for two weeks. Both serum and liver were collected at the end of the feeding trial for biochemistry, histology, and NF-E2-related nuclear factor 2 (NRF2)/antioxidant response element (ARE) signaling analysis. Compared with Control, the AFB treatment caused liver injury and decreased ( < 0.05) body weight gain, feed intake, feed conversion ratio, and serum albumin and total protein by 6.2-20.7%. AFB also induced swelling, necrosis, and severe vacuolar degeneration in chicks' livers. Notably, HD supplementation at 500 and 1000 mg/kg mitigated ( < 0.05) the alterations induced by AFB. HD supplementation alleviated ( < 0.05) AFB-induced impairment in hepatic glutathione peroxidase activity, protein carbonyl, and exo-AFB-8,9-epoxide (AFBO)-DNA concentrations by 57.7-100% and increased ( < 0.05) the activities of superoxide dismutase and catalase by 23.1-40.9% more than those of AFB treatment alone. Furthermore, HD supplementation at the two doses upregulated ( < 0.05) NRF2, NAD(P)H: quinone oxidoreductase-1, heme oxygenase-1, glutathione cysteine ligase catalytic subunit, and glutathione-S transferase A2 and A3 in livers relative to the AFB group by 0.99-3.4-fold. Overall, dietary supplementation of HD at a high dose displayed better protection effects against aflatoxicosis. In conclusion, a dietary HD supplementation at 500 and 1000 mg/kg protected broilers from AFB-induced hepatotoxicity, potentially due to the activation of NRF2/ARE signaling in the chicks.