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.

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.

This study was designed to elucidate the protective effects of resveratrol as a dietary functional factor against HFD-induced testicular injury, with a specific focus on its modulation of the gut microbiota–testis metabolic axis.

This study aimed to investigate the protective effects of compound probiotics (CP) comprising Saccharomyces cerevisiae, Lactobacillus casei, and Bacillus subtilis against aflatoxin B₁ (AFB₁) -induced reproductive toxicity in mice. Kunming mice (n = 60; male) were randomly assigned to six groups and treated via gavage for 28 d with control, AFB₁ alone (150 μg/kg), medium-dose CP (MCP) alone, or AFB₁ combined with low-, medium-, or high-dose CP. Notably, AFB₁ exposure significantly increased the integrated biomarker response version 2 individual (IBRv2i) value to 9.78, whereas medium- and high-dose CP reduced it to 3.59 and 3.22, respectively (P < 0.05), with no significant difference between the MCP and HCP groups (P > 0.05). This identified MCP (1.0 × 10⁶ CFU/mL of each strain) as the minimum effective dose. AFB₁ exposure disrupted gut microbiota by enriching opportunistic pathogens (Staphylococcus, Atopostipes) and altered the testicular metabolome by elevating indoleacetic acid and adenosine. These disturbances impaired spermatogenesis, as evidenced by downregulated meiotic marker SYCP3 alongside upregulated germ cell marker VASA, indicating meiotic arrest with accumulation of undifferentiated germ cells. Mechanistically, AFB₁ inhibited the testicular PI3K/AKT/NRF2 pathway, inducing oxidative stress and apoptosis. Conversely, MCP intervention remodeled gut microbiota by enriching beneficial bacteria (Lactobacillus, Carnobacterium), elevated testicular antioxidant metabolites including 2-n-propylthiazolidine-4-carboxylic acid (PTCA) and L-cysteine, and activated the NRF2/p62 pathway, thereby restoring spermatogenic progression and reversing meiotic arrest. These findings offer new insights into probiotic interventions for environmental reproductive toxicity and highlight PTCA as a potential key signaling molecule in the "gut-testis axis" metabolic communication.

Aflatoxin B₁ (AFB₁) is one of the most dangerous mycotoxins for humans and animals. This study aimed to investigate the effects of compound probiotics (CP), CP supernatant (CPS), AFB₁-degradation enzyme (ADE) on chicken embryo primary intestinal epithelium, liver and kidney cell viabilities, and to determine the functions of CP + ADE (CPADE) or CPS + ADE (CPSADE) for alleviating cytotoxicity induced by AFB₁. The results showed that AFB₁ decreased cell viabilities in dose-dependent and time-dependent manner. The optimal AFB₁ concentrations and reactive time for establishing cell damage models were 200 µg/L AFB₁ and 12 h for intestinal epithelium cells, 40 µg/L and 12 h for liver and kidney cells. Cell viabilities reached 231.58% (p < 0.05) for intestinal epithelium cells with CP addition, 105.29% and 115.84% (p < 0.05) for kidney and liver cells with CPS additions. The further results showed that intestinal epithelium, liver and kidney cell viabilities were significantly decreased to 87.12%, 88.7% and 84.19% (p < 0.05) when the cells were exposed to AFB₁; however, they were increased to 93.49% by CPADE addition, 102.33% and 94.71% by CPSADE additions (p < 0.05). The relative mRNA abundances of IL-6, IL-8, TNF-α, iNOS, NF-κB, NOD1 (except liver cell) and TLR2 in three kinds of primary cells were significantly down-regulated by CPADE or CPSADE addition, compared with single AFB₁ group (p < 0.05), indicating that CPADE or CPSADE addition could alleviate cell cytotoxicity and inflammation induced by AFB₁ exposure through suppressing the activations of NF-κB, NOD1 and TLR2 pathways.