Fusarium mycotoxins are one of the largest families of mycotoxins. Among these mycotoxins, deoxynivalenol is the most widespread pollutant of grains. However, the mechanism underlying the effect of deoxynivalenol on cytotoxicity in human brain endothelial cells was still unclear. This study examined whether deoxynivalenol induced oxidative stress-associated cytotoxicity in primary human brain endothelial cells (HBEC-5i), and explored whether Vitamin E (VE), a selective antioxidant, had protective effects on deoxynivalenol-treated cells. Deoxynivalenol (10-50 μM) concentration-dependently induced cytotoxicity in HBEC-5i cells. Deoxynivalenol (IC50 = 20 μM) activated mitochondrial apoptotic pathway by modulating antioxidant protein expressions (Nrf2, HO-1 and NQO1). More significantly, pre-treatment with VE (20 μM) attenuated the deoxynivalenol-induced cytotoxicity in this cell model. Together, VE significantly alleviated the apoptotic effects of deoxynivalenol in HBEC-5i cells suggesting that it protected the cells against deoxynivalenol-induced oxidative damage. Our findings provided new insight that VE had the potential to ameliorate neurotoxicity of deoxynivalenol.

中文翻译：

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维生素 E 对霉菌毒素脱氧雪腐镰刀菌烯醇诱导的氧化应激及其相关细胞毒性在原代人脑内皮细胞中的保护作用机制

镰刀菌霉菌毒素是最大的霉菌毒素家族之一。在这些霉菌毒素中，脱氧雪腐镰刀菌烯醇是谷物中分布最广的污染物。然而，脱氧雪腐镰刀菌烯醇对人脑内皮细胞细胞毒性影响的机制尚不清楚。该研究检查了脱氧雪腐镰刀菌烯醇是否在原代人脑内皮细胞 (HBEC-5i) 中诱导氧化应激相关的细胞毒性，并探讨了选择性抗氧化剂维生素 E (VE) 是否对脱氧雪腐镰刀菌烯醇处理的细胞具有保护作用。在 HBEC-5i 细胞中，脱氧雪腐镰刀菌烯醇 (10-50 μM) 浓度依赖性地诱导细胞毒性。脱氧雪腐镰刀菌烯醇 (IC50 = 20 μM) 通过调节抗氧化蛋白表达（Nrf2、HO-1 和 NQO1）激活线粒体凋亡途径。更重要的是，在该细胞模型中，用 VE (20 μM) 预处理减弱了脱氧雪腐镰刀菌烯醇诱导的细胞毒性。总之，VE 显着减轻了脱氧雪腐镰刀菌烯醇在 HBEC-5i 细胞中的凋亡作用，表明它保护细胞免受脱氧雪腐镰刀菌烯醇诱导的氧化损伤。我们的研究结果提供了新的见解，即 VE 有可能改善脱氧雪腐镰刀菌烯醇的神经毒性。