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δ-Tocotrienol Suppresses VEGF Induced Angiogenesis whereas α-Tocopherol Does Not

机译:δ-生育三烯酚可抑制VEGF诱导的血管生成,而α-生育酚则不

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Recently, tocotrienol (T3), a less well-known form of vitamin E, has gained considerable attention as a potent antiangiogenic agent. However, the majority of vitamin E research has focused on tocopherol (T_(oc)), with some studies indicating α-Toc may prevent tumor angiogenesis. In this study, we aimed to clarify the differences in antiangiogenic potential between δ-T3 and α-Toc. We showed δ-T3 (2.5-5 μM) completely abolished proliferation, migration and tube formation of human umbilical vein endothelial cells (HUVECs), whereas a similar dose of α-Toc had no such effects. δ-T3 suppressed VEGF receptor 2 (VEGFR-2) signaling, and activated caspases in HUVECs. In addition, via an in vivo mouse Matrigel plug angiogenesis assay, we found that δ-T3 (30 μg), but not α-Toc, inhibited tumor cell-induced vessel formation. In summary, our results demonstrate δ-T3 has superior antiangiogenic activities to α-Toc, and provide insights into the different mechanisms responsible for this effect of T3 and Toc.
机译:最近,作为一种有效的抗血管生成剂,生育三烯酚(T3),一种鲜为人知的维生素E,已经引起了广泛的关注。但是,大多数维生素E的研究都集中在生育酚(T_(oc))上,一些研究表明α-Toc可能会阻止肿瘤血管生成。在这项研究中,我们旨在阐明δ-T3和α-Toc在抗血管生成潜能方面的差异。我们显示δ-T3(2.5-5μM)完全消除了人脐静脉内皮细胞(HUVEC)的增殖,迁移和管形成,而相似剂量的α-Toc没有这种作用。 δ-T3抑制VEGF受体2(VEGFR-2)信号传导,并激活HUVEC中的胱天蛋白酶。另外,通过体内小鼠基质胶栓塞血管生成测定法,我们发现δ-T3(30μg)而非α-Toc抑制了肿瘤细胞诱导的血管形成。总之,我们的结果表明,δ-T3具有比α-Toc更高的抗血管生成活性,并提供了了解造成T3和Toc效应的不同机制的见解。

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