The aim of this study was to evaluate the effects of compound mycotoxin detoxifier (CMD) on alleviating the toxic effect of aflatoxin B₁ (AFB₁) for broiler growth performance. One-kilogram CMD consists of 667 g aflatoxin B₁-degrading enzyme (ADE, 1,467 U/g), 200 g montmorillonite and 133 g compound probiotics (CP). The feeding experiment was divided into 2 stages (1-21 d and 22-42 d). In the early stage, a total of 300 one-day-old Ross broilers were randomly divided into 6 groups, 5 replications for each group, 10 broilers (half male and half female) in each replication. In the later feeding stage, about 240 twenty-two-day-old Ross broilers were randomly divided into 6 groups, 8 replications for each group, 5 broilers in each replication. Group A: basal diet; group B: basal diet with 40 μg/kg AFB₁; group C: basal diet with 1 g/kg CMD; groups D, E, and F: basal diet with 40 μg/kg AFB₁ plus 0.5, 1.0 and 1.5 g/kg CMD, respectively. The results indicated that AFB₁ significantly decreased average daily gain (ADG), protein metabolic rate, organ index of thymus, bursa of Fabricius (BF), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and catalase activities in serum, and increased AFB₁ residues in serum and liver (P < 0.05). Hematoxylin-Eosin (HE) staining analysis of jejunum, liver and kidney showed that AFB₁ caused the main pathological changes with different degrees of inflammatory cell infiltration. However, CMD additions could alleviate the negative effects of AFB₁ on the above parameters. The gut microbiota analysis indicated that AFB₁ could significantly increase the abundances of Staphylococcus-xylosu, Esherichia-coli-g-Escherichia-Shigella, and decrease Lactobacillus-aviarius abundance (P < 0.05), but which were adjusted to almost the same levels as the control group by CMD addition. The correlative analysis showed that Lactobacillus-aviarius abundance was positively correlated with ADG, SOD and BF (P < 0.05), whereas Staphylococcus-xylosus abundance was positively correlated with AFB₁ residues in serum and liver (P < 0.05). In conclusion, CMD could keep gut microbiota stable, alleviate histological lesions, increase growth performance, and reduce mycotoxin toxicity. The optimal CMD addition should be 1 g/kg in AFB₁-contaminated broilers diet.

Deoxynivalenol (DON) is extensively detected in many kinds of foods and feeds to harm human and animal health. This research aims to investigate the effect of chlorogenic acid (CGA) on alleviating inflammation and apoptosis of swine jejunal epithelial cells (IPEC-J2) triggered by DON. The results demonstrated that cell viability was decreased when DON concentrations increased or incubation time expanded. The pretreatment with CGA (40 μg/mL) for 1 h increased cell viability, decreased lactate dehydrogenase (LDH) release and apoptosis in cells triggered by DON at 0.5 μg/mL for 6 h, compared with the DON alone-treated cells. Moreover, the mRNA abundances of IL-8, IL-6, TNF-α, COX-2, caspase-3, Bax and ASCT2 genes, and protein expressions of COX-2, Bax and ASCT2 were significantly down-regulated; while the mRNA abundances of ZO-1, claudin-1, occludin, PePT1 and GLUT2 genes, and protein expressions of ZO-1, claudin-1 and PePT1 were significantly up-regulated in the CGA + DON group, compared with the DON alone group. This study indicated that CGA pretreatment alleviated cytotoxicity, inflammation and apoptosis in DON-triggered IPEC-J2 cells, and protected intestinal cell integrity from DON damages.

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.

Aflatoxins B1 (AFB1), deoxynivalenol (DON) and zearalenone (ZEA) are the three most prevalent mycotoxins, whose contamination of food and feed is a severe worldwide problem. In order to alleviate the toxic effects of multi-mycotoxins (AFB1 + DON + ZEA, ADZ) on inflammation and apoptosis in swine jejunal epithelial cells (IPEC-J2), three species of probiotics (Bacillus subtilis, Saccharomyces cerevisiae and Pseudomonas lactis at 1 × 10⁵ CFU/mL, respectively) were mixed together to make compound probiotics (CP), which were further combined with 400 μg/mL of glycyrrhinic acid (GA) to make bioactive materials (CGA). The experiment was divided into four groups, i.e., the control, ADZ, CGA and ADZ + CGA groups. The results showed that ADZ decreased cell viability and induced cytotoxicity, while CGA addition could alleviate ADZ-induced cytotoxicity. Moreover, the mRNA expressions of IL-8, TNF-α, NF-Κb, Bcl-2, Caspase-3, ZO-1, Occludin, Claudin-1 and ASCT2 genes, and protein expressions of TNF-α and Claudin-1 were significantly upregulated in ADZ group; while the mRNA abundances of IL-8, TNF-α, NF-Κb, Caspase-3, ASCT2 genes, and protein expressions of TNF-α and Claudin-1 were significantly downregulated in the ADZ + CGA group. In addition, the protein expressions of COX-2, ZO-1, and ASCT2 were significantly downregulated in the ADZ group, compared with the control group; whereas CGA co-incubation with ADZ could increase these protein expressions to recover to normal levels. This study indicated that CGA could alleviate cytotoxicity, apoptosis and inflammation in ADZ-induced IPEC-J2 cells and protect intestinal cell integrity from ADZ damages.

This study aimed to assess how the bacterial–enzyme co-fermentation of corn straw affects fermentation quality, the digestion rate in Hu sheep, and rumen microorganisms. Orthogonal experiments were utilized to establish the optimal fermentation conditions, which were subsequently applied in bacterial–enzyme fermentation trials involving four groups: group A (control), group B (enzyme added), group C (bacteria added), and group D (bacteria + enzyme). The results show that the optimal fermentation conditions were the addition of 2% corn flour, 2% cottonseed meal, and 60% moisture. In comparison with group A, group D demonstrated the most favorable outcomes, notably reducing the pH and cellulose content while enhancing the lactic acid content. The relative abundances of Pantoea and Weissella reduced, whereas those of Lactiplantibacillus and Limosilactobacillus increased, in the fermented corn straw. In the animal experiments, group D exhibited significantly higher digestibility of NDF and ADF; total VFA, acetic acid, and NH₃-N contents; and enzyme activity compared with groups A and B. Additionally, the relative abundances of Prevotella, NK4A214-group, Entodinium, and Polyplastron increased, while those of Dasytricha and Enoploplastron decreased, in group D compared with group A. It can be concluded that Lactobacillus plantarum and cellulase treatments enhance the nutritional value of corn straw by improving ruminal fermentation and regulating the sheep rumen microbiota.