Deoxynivalenol (DON), as a widespread Fusarium mycotoxin in cereals, food products, and animal feed, is detrimental to both human and animal health. The liver is not only the primary organ responsible for DON metabolism but also the principal organ affected by DON toxicity. Taurine is well known to display various physiological and pharmacological functions due to its antioxidant and anti-inflammatory properties. However, the information regarding taurine supplementation counteracting DON-induced liver injury in piglets is still unclear. In our work, twenty-four weaned piglets were subjected to four groups for a 24-day period, including the BD group (a basal diet), the DON group (3 mg/kg DON-contaminated diet), the DON+LT group (3 mg/kg DON-contaminated diet + 0.3% taurine), and the DON+HT group (3 mg/kg DON-contaminated diet + 0.6% taurine). Our findings indicated that taurine supplementation improved growth performance and alleviated DON-induced liver injury, as evidenced by the reduced pathological and serum biochemical changes (ALT, AST, ALP, and LDH), especially in the group with the 0.3% taurine. Taurine could counteract hepatic oxidative stress in piglets exposed to DON, as it reduced ROS, 8-OHdG, and MDA concentrations and improved the activity of antioxidant enzymes. Concurrently, taurine was observed to upregulate the expression of key factors involved in mitochondrial function and the Nrf2 signaling pathway. Furthermore, taurine treatment effectively attenuated DON-induced hepatocyte apoptosis, as verified through the decreased proportion of TUNEL-positive cells and regulation of the mitochondria-mediated apoptosis pathway. Finally, the administration of taurine was able to reduce liver inflammation due to DON, by inactivating the NF-κB signaling pathway and declining the production of pro-inflammatory cytokines. In summary, our results implied that taurine effectively improved DON-induced liver injury. The underlying mechanism should be that taurine restored mitochondrial normal function and antagonized oxidative stress, thereby reducing apoptosis and inflammatory responses in the liver of weaned piglets.

Deoxynivalenol (DON) is a prevalent foodborne contaminant present in crops, posing significant risks to food safety and public health worldwide. Mitochondria, as the primary target of DON, play a crucial role in DON-mediated gastrointestinal toxicity. Taurine, a multifunctional nutrient, has been reported to exert antioxidant and anti-inflammatory effects by modulating mitochondrial function. However, whether taurine could alleviate intestinal injury by restoring mitochondrial function under DON exposure remains unclear. To address this knowledge gap, this study systematically investigated the potential protective effects of taurine on DON-induced intestinal damage in a piglet model. Twenty-four piglets were randomly assigned to four groups for 24 days: BD group (basal diet), DON group (3 mg/kg DON-contaminated diet), DON+LT group (DON diet with 0.3 % taurine), and DON+HT group (DON diet with 0.6 % taurine). Serum samples were collected for biochemical analysis, while jejunal tissues were examined for histology, barrier function, oxidative stress, inflammation, apoptosis, mitochondrial function, as well as related gene and protein expression. The results revealed that taurine effectively restored jejunal morphology disrupted by DON, as evidenced by increases in villus height/width and the villus height to crypt depth ratio. It preserved intestinal barrier integrity, reflected by reductions in diamine oxidase and D-lactate levels, alongside increased expression of genes and proteins related to intestinal mucus and mechanical barrier function. Furthermore, taurine mitigated intestinal oxidative stress by reducing reactive oxygen species, 8-hydroxydeoxyguanosine, and malondialdehyde levels, while enhancing antioxidant defenses. It also alleviated inflammation by suppressing pro-inflammatory cytokines and attenuated intestinal epithelial apoptosis through mitochondrial caspase-dependent and apoptosis-inducing factor-mediated pathways. Intriguingly, taurine improved the damaged mitochondrial structure and functionality within the intestinal epithelium irritated by DON. This improvement included enhanced respiratory chain complex activity, increased ATP levels, and mtDNA copy number. Additionally, taurine regulated gene expression related to mitochondrial respiration, fusion, fission, and autophagy. Simultaneously, taurine reversed the DON-induced inhibition of the peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC1α)-nuclear respiratory factor 1/2 (NRF1/2) axis, a critical pathway regulating mitochondrial biogenesis, respiratory function, and oxidative stress responses. Correlation analysis revealed significant associations between the PGC1α-NRF1/2 axis and mitochondrial function, as well as correlations with intestinal health parameters, including barrier function, redox status, inflammation, and apoptosis. In summary, this study provides the first evidence that dietary taurine supplementation effectively alleviates intestinal injury in DON-challenged piglets through mitochondrial restoration, which is strongly associated with the reactivation of the PGC1α-NRF1/2 axis. Our findings highlight the potential of mitochondrial-targeted therapies to mitigate gastrointestinal toxicity caused by the foodborne contaminant DON in both humans and animals.

Transition dairy cows face severe oxidative stress that disrupts mammary epithelial homeostasis through intertwined oxidative, inflammatory, and endoplasmic reticulum (ER) stress pathways. This study hypothesized that rutin, a natural flavonoid, alleviates hydrogen peroxide (H₂O₂)-induced oxidative damage in bovine mammary epithelial cells (BMECs) via AMPK/NFE2L2 signaling activation. In this study, BMECs were pre-incubated with rutin. Subsequently, cells were treated with or without H₂O₂. Additionally, by transfecting BMECs with NFE2L2 siRNA (siNFE2L2), we investigated how AMPK/NFE2L2 signaling mediated by rutin may prevent H₂O₂-induced oxidative damage. The results show that increases in reactive oxygen species (ROS), expression of inflammatory cytokines, expression of proteins related to endoplasmic reticulum stress and the apoptosis rate induced by H₂O₂ in cells, were attenuated in rutin cultures. Challenges with H₂O₂ led to a lower abundance of proteins related to AMPK and NFE2L2. Comparatively, these effects were reversed in cultures with rutin. Transfection with siNFE2L2 reversed the protection of rutin, suggesting that NFE2L2 is essential for the protective mechanism of rutin. These results elucidated the molecular mechanism of rutin’s resistance to H₂O₂-mediated oxidative injury through the AMPK/NFE2L2 signaling pathway and suggested that it could be used as a potent in vivo antioxidant for ruminants during periods of stress, such as before and after calving.