杨梅素通过诱导内皮细胞凋亡和抑制PI3K/Akt/mTOR信号通路来抑制血管生成。
Myricetin Inhibits Angiogenesis by Inducing Apoptosis and Suppressing PI3K/Akt/mTOR Signaling in Endothelial Cells.
作者信息
Kim Gi Dae
机构信息
Department of Food, Nutrition and Biotechnology, Kyungnam University, Changwon, Korea.
出版信息
J Cancer Prev. 2017 Dec;22(4):219-227. doi: 10.15430/JCP.2017.22.4.219. Epub 2017 Dec 30.
BACKGROUND
Myricetin has been shown to possess potential antiangiogenic effects in endothelial cells. However, the underlying mechanisms are not fully understood. Therefore, we evaluated its antiangiogenic effects in human umbilical vascular endothelial cells (HUVECs).
METHODS
HUVECs were cultured in endothelial cell growth medium-2 to induce proliferation and angiogenesis and treated with different doses of myricetin (0.25, 0.5, and 1 μM) for 24 hours. Cell proliferation was analyzed by the MTT and lactate dehydrogenase release assays; angiogenesis was determined by the tube formation assay. In addition, cell signaling pathways related to angiogenesis were investigated by Western blotting.
RESULTS
Myricetin induced apoptosis and procaspase-3 cleavage though the induction of reactive oxygen species (ROS). It significantly inhibited cell migration, tube formation, and PI3K/Akt/mTOR signaling in HUVECs.
CONCLUSIONS
Myricetin exerts antiangiogenic effects by inducing ROS-mediated apoptosis and inhibiting PI3K/Akt/mTOR signaling in HUVECs.
背景
杨梅素已被证明在内皮细胞中具有潜在的抗血管生成作用。然而，其潜在机制尚未完全明确。因此，我们评估了杨梅素对人脐静脉血管内皮细胞（HUVECs）的抗血管生成作用。
方法
将HUVECs培养于内皮细胞生长培养基 - 2中以诱导增殖和血管生成，并用不同剂量的杨梅素（0.25、0.5和1 μM）处理24小时。通过MTT和乳酸脱氢酶释放试验分析细胞增殖；通过管腔形成试验测定血管生成。此外，通过蛋白质印迹法研究与血管生成相关的细胞信号通路。
结果
杨梅素通过诱导活性氧（ROS）诱导细胞凋亡和前半胱天冬酶 - 3裂解。它显著抑制HUVECs中的细胞迁移、管腔形成以及PI3K/Akt/mTOR信号传导。
结论
杨梅素通过诱导ROS介导的细胞凋亡并抑制HUVECs中的PI3K/Akt/mTOR信号传导发挥抗血管生成作用。
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