Taurine alleviated paraquat-induced oxidative stress and gut-liver axis damage in weaned piglets by regulating the Nrf2/Keap1 and TLR4/NF-κB signaling pathways

作者：Chen Chen, Min Qi, Weilong Zhang, Fanxing Chen, Zhihong Sun, Weizhong Sun, Wenjie Tang, Zhenguo Yang, Xuan Zhao, Zhiru Tang · 发表于：Journal of Animal Science and Biotechnology/Journal of animal science and biotechnology · 年份：2025 · DOI：10.1186/s40104-025-01244-3 · 被引用次数：9 · 研究领域：Paraquat toxicity studies and treatments、Aldose Reductase and Taurine、Paraoxonase enzyme and polymorphisms

BACKGROUND: Oxidative stress can impair intestinal barrier function and cause liver damage, resulting in reduced animal productivity. Paraquat (PQ) induces significant oxidative stress in weaned piglets. The antioxidant, anti-inflammatory, and metabolic regulatory functions of taurine (Tau), a free amino acid that is widely distributed in the body, have been extensively studied. However, the mechanisms by which dietary Tau alleviates oxidative stress and gut-liver axis damage in weaned piglets remain unclear. METHODS: Forty weaned piglets (20 males and 20 females; 6.41 ± 0.11 kg; 25 days old; Duroc × Landrace × Yorkshire) were used in a 2 × 2 factorial design to investigate the mechanism by which dietary Tau (0% or 0.4%) alleviates PQ-induced oxidative stress and gut-liver axis damage. We analyzed key biomarkers related to gut barrier function, mucosal damage repair, liver damage, gut-liver immunity, antioxidant capacity, systemic immune homeostasis, antioxidant levels, and gut microbiota diversity in piglets under normal and acute oxidative stress. In particular, we evaluated the coordinated regulation of gut-liver axis function mediated by Tau through the Nrf2/Keap1 (antioxidant) and TLR4/NF-κB (immune modulation) signaling pathways. Partial least squares path modeling and molecular docking were used to explore the intrinsic relationship between PQ, Tau, and the gut-liver axis. RESULTS: PQ exposure impaired gut barrier function, increased the liver fibrosis area, and marked...