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Dietary taurine supplementation counteracts deoxynivalenol-induced liver injury via alleviating oxidative stress, mitochondrial dysfunction, apoptosis, and inflammation in piglets

文献类型： 外文期刊

作者： Ji, Xu 1 ; Tang, Zhongqi 2 ; Zhang, Feng 2 ; Zhou, Fen 1 ; Wu, Yijing 1 ; Wu, Dong 1 ;

作者机构： 1.Anhui Acad Agr Sci, Inst Anim Sci & Vet Med, Anhui Prov Key Lab Livestock & Poultry Prod Safety, Hefei 230001, Peoples R China

2.Anhui Sci & Technol Univ, Coll Anim Sci, Chuzhou 233100, Peoples R China

3.Anhui Prov Key Lab Anim Nutr Regulat & Hlth, Chuzhou 233100, Peoples R China

4.Fengyang Xiaogang Minyi Land Shares Cooperat, Chuzhou 233100, Peoples R China

5.Anhui Acad Agr Sci, Inst Anim Sci & Vet Med, 40 Nongke South Rd, Hefei 230001, Peoples R China

关键词： Deoxynivalenol; Taurine; Liver injury; Oxidative stress; Apoptosis; Inflammation

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.8； 五年影响因子：6.9 ）

ISSN： 0147-6513

年卷期： 2023 年 253 卷

页码：

收录情况： SCI

摘要： 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 DONcontaminated 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 DONinduced 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-kappa B signaling pathway and declining the production of proinflammatory 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.

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