Vitamin E, a fat-soluble compound, possesses both antioxidant and non-antioxidant properties. In this study we evaluated, in intestinal HT29 cells, the role of natural tocopherols, α-Toc and δ-Toc, and two semi-synthetic derivatives, namely bis-δ-Toc sulfide (δ-Toc)₂S and bis-δ-Toc disulfide (δ-Toc)₂S₂, on TNFα-induced oxidative stress, and intercellular adhesion molecule-1 (ICAM-1) and claudin-2 (Cl-2) expression. The role of tocopherols was compared to that of N-acetylcysteine (NAC), an antioxidant precursor of glutathione synthesis. The results show that all tocopherol containing derivatives used, prevented TNFα-induced oxidative stress and the increase of ICAM-1 and Cl-2 expression, and that (δ-Toc)₂S and (δ-Toc)₂S₂ are more effective than δ-Toc and α-Toc. The beneficial effects demonstrated were due to tocopherol antioxidant properties, but suppression of TNFα-induced Cl-2 expression seems not only to be related with antioxidant ability. Indeed, while ICAM-1 expression is strongly related to the intracellular redox state, Cl-2 expression is TNFα-up-regulated by both redox and non-redox dependent mechanisms. Since ICAM-1 and Cl-2 increase intestinal bowel diseases, and cause excessive recruitment of immune cells and alteration of the intestinal barrier, natural and, above all, semi-synthetic tocopherols may have a potential role as a therapeutic support against intestinal chronic inflammation, in which TNFα represents an important proinflammatory mediator.

中文翻译：

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天然和半合成生育酚对HT29肠上皮细胞中TNFα诱导的ROS产生以及ICAM-1和Cl-2表达的保护作用

维生素E，脂溶性化合物，具有抗氧化剂和非抗氧化剂的特性。在这项研究中，我们评估了肠道HT29细胞中天然生育酚α-Toc和δ-Toc以及两种半合成衍生物bis - δ-Toc硫化物（δ-Toc）₂ S和bis- δ的作用。 -Toc二硫化物（δ-Toc）₂ S ₂对TNFα诱导的氧化应激，以及细胞间粘附分子1（ICAM-1）和claudin-2（Cl-2）的表达。比较了生育酚和氮的作用-乙酰半胱氨酸（NAC），谷胱甘肽合成的抗氧化剂前体。结果表明，所有使用的生育酚衍生物均能防止TNFα诱导的氧化应激以及ICAM-1和Cl-2表达的增加，并且（δ-Toc）₂ S和（δ-Toc）₂ S ₂更有效。比δ-Toc和α-Toc。所显示的有益作用是由于生育酚的抗氧化特性，但抑制TNFα诱导的Cl-2表达似乎不仅与抗氧化能力有关。实际上，尽管ICAM-1表达与细胞内氧化还原状态密切相关，但Cl-2表达却受氧化还原和非氧化还原依赖性机制的TNFα上调。由于ICAM-1和Cl-2会增加肠道肠道疾病，并导致免疫细胞过度募集和肠道屏障改变，因此天然的，尤其是半合成的生育酚可能具有潜在的作用，可作为抵抗肠道慢性炎症的治疗支持，其中TNFα代表重要的促炎介质。