Shenzhen Key Laboratory of Edible and Medicinal Bioresources, Hong Kong University of Science and Technology (HKUST) Shenzhen Research Institute, Shenzhen, China.
Division of Life Science, Center for Chinese Medicine, State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology, Hong Kong, China; and.
FASEB J. 2019 Jan;33(1):532-544. doi: 10.1096/fj.201800750R. Epub 2018 Jul 10.
Polydatin, also called piceid, is a stilbenoid glucoside of a resveratrol derivative. It derives mainly from the root and rhizome of Polygonum cuspidatum Sieb. et Zucc. Although the role of P. cuspidatum root in angiogenesis has been reported, the active chemical or chemicals responsible for such function is not known. Here, polydatin was proposed to bind VEGF, which therefore altered the functions of VEGF in angiogenesis. Several lines of evidence supported the pharmaceutical effects of polydatin in VEGF-induced angiogenesis. In human umbilical vein endothelial cells, polydatin inhibited VEGF-stimulated cell proliferation, cell migration, and tube formation. Moreover, polydatin showed suppressive effects on the subintestinal vessel formation in zebrafish embryos. In signaling cascades, polydatin application attenuated VEGF-induced phosphorylations of VEGF receptor 2 and JNK. Moreover, the VEGF-induced phosphorylations of Akt, eNOS, and Erk were significantly decreased in the presence of polydatin. In parallel, the formation of reactive oxygen species, triggered by VEGF, was markedly decreased under polydatin application. Thus, our results supported the angiogenic roles of polydatin, as well as its signaling mechanism in blocking VEGF-mediated responses. The current study provides support for the possible development of polydatin as a potential therapeutic agent for treatment and prevention of angiogenesis-related diseases.-Hu, W.-H., Wang, H.-Y., Kong, X.-P., Xiong, Q.-P., Poon, K. K.-M., Xu, L., Duan, R., Chan, G. K.-L., Dong, T. T.-X., Tsim, K. W.-K. Polydatin suppresses VEGF-induced angiogenesis through binding with VEGF and inhibiting its receptor signaling.
虎杖苷，也称为白藜芦醇苷，是白藜芦醇衍生物的一种芪类葡萄糖苷。它主要来源于虎杖的根和根茎。虽然已经报道了虎杖根在血管生成中的作用，但负责这种功能的活性化学物质或化学物质尚不清楚。在这里，我们提出虎杖苷与 VEGF 结合，从而改变了 VEGF 在血管生成中的功能。有几条证据支持虎杖苷在 VEGF 诱导的血管生成中的药物作用。在人脐静脉内皮细胞中，虎杖苷抑制 VEGF 刺激的细胞增殖、细胞迁移和管形成。此外，虎杖苷在斑马鱼胚胎中显示出对亚肠道血管形成的抑制作用。在信号级联中，虎杖苷应用减弱了 VEGF 诱导的 VEGFR2 和 JNK 的磷酸化。此外，在虎杖苷存在的情况下，VEGF 诱导的 Akt、eNOS 和 Erk 的磷酸化显著减少。同时，VEGF 触发的活性氧的形成在虎杖苷应用下明显减少。因此，我们的结果支持虎杖苷的血管生成作用，以及其在阻断 VEGF 介导的反应中的信号机制。本研究为虎杖苷作为治疗和预防与血管生成相关疾病的潜在治疗剂的可能发展提供了支持。-Hu, W.-H., Wang, H.-Y., Kong, X.-P., Xiong, Q.-P., Poon, K. K.-M., Xu, L., Duan, R., Chan, G. K.-L., Dong, T. T.-X., Tsim, K. W.-K. 虎杖苷通过与 VEGF 结合并抑制其受体信号抑制 VEGF 诱导的血管生成。
