T‐2 toxin is a trichothecene mycotoxin and is considered as an extremely inevitable pollutant with potent hepatotoxicity. However, the approach to alleviation of T‐2 toxin‐triggered hepatotoxicity has been recognized as a serious challenge. Resveratrol (Res) is a polyphenol natural product isolated from various plant species, but its protective effect against T‐2 toxin hepatotoxicity and detailed mechanism remains obscure. In the present study, the effect of Res against the hepatotoxicity was evaluated, and the underlying mechanisms were further revealed in mice. Functionally, Res inhibited liver injury, oxidative damage, and mitochondrial dysfunction induced by T‐2 toxin. Mechanistically, Res modulated Nrf2‐mediated antioxidant pathway and glutathione synthesis inhibition. Collectively, our findings first showed beyond doubt that Res ameliorated T‐2 toxin‐triggered liver injury by regulating Nrf2 pathways in mice.

中文翻译：

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白藜芦醇通过保留 Nrf2 通路和 GSH 合成减轻 T-2 毒素诱导的肝损伤


T-2 毒素是一种单端孢霉烯类霉菌毒素，被认为是一种极其不可避免的污染物，具有强大的肝毒性。然而，减轻 T-2 毒素触发的肝毒性的方法已被公认为一个严峻的挑战。白藜芦醇 （Res） 是一种从各种植物物种中分离的多酚天然产物，但其对 T-2 毒素肝毒性的保护作用和详细机制仍不清楚。在本研究中，评估了 Res 对肝毒性的影响，并在小鼠中进一步揭示了潜在机制。在功能上，Res 抑制 T-2 毒素诱导的肝损伤、氧化损伤和线粒体功能障碍。从机制上讲，Res 调节 Nrf2 介导的抗氧化途径和谷胱甘肽合成抑制。总的来说，我们的研究结果首先毫无疑问地表明，Res 通过调节小鼠的 Nrf2 通路改善了 T-2 毒素触发的肝损伤。