Abstract
In order to alleviate the toxic effects of aflatoxins B1 (AFB1) on inflammatory responses in the intestine, liver, and kidney of broilers, the aflatoxin B1-degrading enzyme, montmorillonite, and compound probiotics were selected and combined to make a triple-action compound mycotoxin detoxifier (CMD). The feeding experiment was divided into two stages. In the early feeding stage (1−21 day), a total of 200 one-day-old Ross broilers were randomly divided into four groups; in the later feeding stage (22−42 day), 160 broilers aged at 22 days were assigned to four groups: Group A: basal diet (4.31 μg/kg AFB1); Group B: basal diet with 40 μg/kg AFB1; Group C: Group A plus 1.5 g/kg CMD; Group D: Group B plus 1.5 g/kg CMD. After the feeding experiment, the intestine, liver, and kidney tissues of the broilers were selected to investigate the molecular mechanism for CMD to alleviate the tissue damages. Analyses of mRNA abundances and western blotting (WB) of inflammatory factors, as well as immunohistochemical (IHC) staining of intestine, liver, and kidney tissues showed that AFB1 aggravated the inflammatory responses through NF-κB and TN-α signaling pathways via TLR pattern receptors, while the addition of CMD significantly inhibited the inflammatory responses. Phylogenetic investigation showed that AFB1 significantly increased interleukin-1 receptor-associated kinase (IRAK-1) and mitogen-activated protein kinase (MAPK) activities (p < 0.05), which were restored to normal levels by CMD addition, indicating that CMD could alleviate cell inflammatory damages induced by AFB1.