Yumei Liu

Previous studies conducted in our laboratory have demonstrated that dietary supplementation with Bacillus coagulans BC66 (BC66) can mitigate intestinal, renal, and hepatic injuries induced by Klebsiella pneumoniae in rabbits. However, the potential of Bacillus coagulans BC66 in protecting against Klebsiella pneumoniae- induced acute lung injury remains unexplored. Therefore, the present study aimed to investigate the protective mechanism of Bacillus coagulans BC66 against acute lung injury induced by Klebsiella pneumoniae in rabbits using histological examination (hematoxylin and eosin staining, HE staining), immunofluorescence, immunohistochemistry and Western blotting. Dietary supplementation with Bacillus coagulans BC66 alleviated acute lung injury in rabbits by reducing inflammatory cell infiltration, alleviating alveolar wall thickening, and minimizing alveolar lumen narrowing. Additionally, BC66 enhanced the pulmonary barrier by upregulating proliferating cell nuclear antigen (PCNA) expression and modulating the levels of tight junction proteins, including Occludin, Claudin-1, and ZO-1. Importantly, BC66 restored T helper 17/regulatory T cell (Th17/Treg) immune balance, which was identified as the central mechanism underlying its protective effects. This immune modulation was associated with reduced production of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), and contributed to the improvement of pulmonary barrier integrity. Furthermore, the regulation of Th17/Treg balance was accompanied by downstream attenuation of oxidative stress and ferroptosis, as evidenced by increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), decreased malondialdehyde (MDA) levels, and modulation of ferroptosis-related proteins, including solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), partly through activation of the Keap1/Nrf2/HO-1 pathway.In conclusion, this study demonstrates that Bacillus coagulans BC66 protects against Klebsiella pneumoniae-induced acute lung injury primarily through restoring Th17/Treg immune balance, with subsequent downstream effects on inflammation, epithelial barrier function, oxidative stress, and ferroptosis. Notably, pretreatment with 1 × 10⁶ colony-forming units per gram (CFU/g) was the most effective. These findings provide a theoretical basis for using Bacillus coagulans BC66 as a preventive agent against acute lung injury induced by Klebsiella pneumoniae in rabbits.

To improve the vitrification efficiency of bovine germinal vesicle (GV) oocytes, the use of hydroxyapatite (HA) nanoparticles as a novel cryopreservation additive represents a promising approach. This study aimed to investigate the effects of HA nanoparticles and permeable cryoprotective agents (CPAs) on the ultrastructure, developmental competence, and gene expression of bovine GV oocytes following vitrification. Oocytes were vitrified in vitrification solutions containing HA nanoparticles of different sizes (20, 40, or 60 nm) and concentrations (0.01%, 0.05%, or 0.1%) to determine the optimal conditions based on survival rate, mitochondrial membrane potential (MMP) level, and developmental competence. Subsequently, the synergistic effects of HA nanoparticles and permeable CPAs (VS: 20% EG + 20% DMSO; VS1: 17.5% EG + 17.5% DMSO) were further evaluated. The optimal treatment (40 nm 0.05% HA nanoparticles) significantly increased MMP level, and improved developmental competence compared with the vitrified control group (p < 0.05). Among the vitrified groups, vitrified oocytes in the VS1-HA group (combining HA nanoparticles with reduced concentrations of permeable CPAs) exhibited the highest MMP level (1.89), maturation rate (50.39%), cleavage rate (27.07%), and blastocyst rate (10.53%) (p < 0.05). Ultrastructural analysis further revealed that the VS1-HA group maintained more intact zona pellucida structures and showed reduced mitochondrial swelling compared with the vitrified control group. Moreover, the expression levels of genes associated with zona pellucida formation (ZP3), mitochondrial fusion (MFN1), and chromatin remodeling (NPM2) were significantly upregulated in the VS1-HA group relative to the vitrified control group. Overall, these findings indicate that the combination of HA nanoparticles with lower concentrations of permeable CPAs enhances MMP level, alleviates vitrification-induced ultrastructural damage, and upregulates the expression of key developmental genes, thereby improving the developmental competence of vitrified bovine GV oocytes.

BACKGROUND: Dietary aflatoxin B1 (AFB1) contamination poses a significant threat to livestock health and food safety by causing severe liver injury. l ‐Aspartic acid ( l ‐Asp) is known for its antioxidant and anti‐inflammatory properties but its potential to mitigate AFB1‐induced hepatotoxicity and associated intestinal dysbiosis in rabbits remains unexplored. To address this, 35‐day‐old rabbits ( n = 50) were assigned randomly to five groups: a control group, an AFB1 (0.3 mg kg ⁻¹ bodyweight) group, and three groups receiving dietary l ‐Asp supplementation (0.5%, 1.0%, or 1.5%) for 21 days, with AFB1 administered during the final 5 days. RESULT: The results demonstrated that l ‐Asp pretreatment significantly alleviated AFB1‐induced impairments in growth performance and serum biochemical parameters. It also reduced hepatic collagen fiber deposition, ameliorated ileal barrier damage, and restored the gut microbiota composition and normalized bile acid metabolism, which correlated with the regulation of key metabolic receptors. CONCLUSION: This study established 1.0% l ‐asp as an effective, gut‐liver axis‐targeted intervention against AFB1 toxicity in rabbits. This work emphasizes its nutritional potential and provides a clear rationale for future studies to elucidate its molecular mechanisms. © 2026 Society of Chemical Industry.

The aim of this study is to explore the protective effect of selenomethionine (SeMet) against the immunotoxicity caused by aflatoxin B1 (AFB1) in male rabbits. Fifty healthy male rabbits aged 90 days were randomly divided into 5 groups: control group, model group, low dose selenomethionine group (Se-1), middle dose selenomethionine group (Se-2) and high dose selenomethionine group (Se-3). The control group and model group were fed basal diet, and the other three groups were fed SeMet 0.2 mg/kg, 0.4 mg/kg and 0.6 mg/kg respectively. On the 31st day of the experiment, All rabbits in the model group and three treatment groups were fed 0.5 mg/kg AFB1 for 21 days. Detect the levels of immune-related indicators in rabbit plasma. Collect samples, and observe the pathological changes in rabbit spleen and sacculus rotundus using hematoxylin-eosin (HE) staining. Analyze the expression of related proteins in spleen and sacculus rotundus tissues using immunofluorescence and Western blot (WB) analysis. Measure the levels of relevant inflammatory factor mRNA in spleen and sacculus rotundus tissues using qRT-PCR. Use enzyme-linked immunosorbent assay (ELISA) to detect the levels of oxidative stress-related indicators and inflammatory factors in spleen and sacculus rotundus tissues. The results indicate that AFB1 can induce oxidative stress and inflammation by activating the TLR-2/NF-κB signaling pathway, inhibiting the proliferation and differentiation of spleen and bursa cells, disrupting the normal structure of the spleen and sacculus rotundus tissues, and reducing the levels of immune-related indicators in plasma. SeMet pretreatment significantly inhibited the TLR-2/NF-κB signaling pathway, alleviating oxidative stress damage in spleen and sacculus rotundus tissues and reducing the inflammatory response in rabbits.Thus, we demonstrate that SeMet mitigates AFB1-induced immunotoxicity in reserve male rabbits by inhibiting the TLR-2/NF-κB signaling pathway. In addition, in this study, the effect of 0.4 mg/kg SeMet was the most effective. SeMet is a natural and safe drug that can prevent AFB1 poisoning in rabbit feed.

Zearalenone (ZEA), a mycotoxin primarily generated by the Fusarium species, constitutes a prevalent contaminant in both human and animal feedstuffs. Chronic exposure to this mycotoxin induces hepatic inflammatory responses in livestock species including rabbits, ultimately leading to organ damage. Selenomethionine (SeMet), an organic selenium source recognized for its antioxidant properties and anti-inflammatory bioactivity, demonstrates protective benefits in animals through its detoxification mechanism and growth promotion. The present study investigated the protective effect of SeMet against ZEA-induced hepatic inflammation and elucidated its underlying mechanisms. Fifty healthy 90-day-old rabbits were randomly divided into five groups: control, ZEA-exposed and three SeMet-supplemented groups receiving 0.2, 0.35 or 0.5 mg/kg via dietary inclusion. After two weeks of SeMet pretreatment, ZEA administration (1.2 mg/kg B.W.) was imitated via oral gavage daily for one week in both the ZEA group and three SeMet-treated groups. As a result, ZEA exposure induced the significant structural disruption of the hepatic lobules, accompanied by increased collagen deposition, elevated pro-inflammatory cytokine profiles (IL-6, IL-1β, TNF-α) and reduced anti-inflammatory mediator levels (IL-10, TGF-β). SeMet supplementation alleviated ZEA-induced histological alterations, including inflammatory cell infiltration and collagen accumulation. Biochemical analysis indicated the restoration of inflammatory markers to near-normal levels when treated with SeMet. Notably, immunohistochemical results showed that SeMet significantly reduced the protein levels of IL-6 and its downstream target STAT3 under ZEA exposure. These findings indicated that SeMet attenuated ZEA-induced hepatic inflammation by modulating the IL-6/STAT3 signaling axis, with dietary supplementation of 0.35 mg/kg SeMet exhibiting the most significant effect on alleviating ZEA-induced hepatic inflammatory injury.

Zearalenone (ZEA) is one of the common mycotoxins in feeds. ZEA and its metabolites have estrogen-like activity and can competitively bind to estrogen receptors, causing reproductive dysfunction and damage to reproductive organs. The toxicity mechanism of ZEA mainly inhibits the antioxidant pathway and antioxidant enzyme activity, induces cell cycle arrest and DNA damage, and blocks the process of cellular autophagy to produce toxic effects. In animal husbandry practice, when animals ingest ZEA-contaminated feed, it is likely to lead to abortion in females, abnormal sperm viability in males with inflammatory reactions in various organs, and cancerous changes in the reproductive organs of humans when they ingest contaminated animal products. In this paper, we reviewed in detail how ZEA induces oxidative damage by inducing the generation of reactive oxygen species (ROS) and regulating the expression of genes related to oxidative pathways, induces germ cell apoptosis through the mitochondrial and death receptor pathways, and activates the expression of genes related to autophagy in order to induce cellular autophagy. In addition, the molecular detoxification mechanism of ZEA is also explored in this paper, aiming to provide a new direction and theoretical basis for the development of new ZEA detoxification methods to better reduce the global pollution and harm caused by ZEA.