EGCG attenuates atherosclerosis through the Jagged-1/Notch pathway.
EGCG attenuates atherosclerosis through the Jagged-1/Notch pathway.
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EGCG 通过 Jagged-1/Notch 通路减轻动脉粥样硬化。
DOI：
10.3892/ijmm.2015.2422
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发表时间：
2016-02
期刊：
影响因子：
--
通讯作者：
Peng Daoquan
中科院分区：
文献类型：
--
作者：
Yin Jianguo;Huang Fang;Yi Yuhong;Yin Liang;Peng Daoquan
动脉粥样硬化是全球心血管疾病最常见的原因。氧化低密度脂蛋白（ox-LDL）是动脉粥样硬化发病机制中一个特别重要的危险因素。越来越多的证据表明，表没食子儿茶素-3-没食子酸酯（EGCG;一种在流行饮料绿茶中发现的儿茶素）可以预防ox-LDL诱导的动脉粥样硬化。然而，其潜在机制仍不清楚。在本研究中，ox-LDL（100 mg/l）通过降低内皮型一氧化氮合酶（eNOS）表达和促进诱导型一氧化氮合酶（iNOS）表达，诱导人脐静脉内皮细胞（HUVECs）损伤和凋亡;这些作用可通过添加50 µM EGCG消除。此外，ox-LDL快速激活p22 phox的膜转位，并改变Jagged-1和Notch途径相关蛋白[Math 1，hairy和分裂增强子（HES）1和HES 5]的蛋白表达;这些作用也被50 µM EGCG预处理所阻止。此外，Jagged-1在EGCG介导的保护作用中发挥了重要作用，防止ox-LDL诱导的HUVECs凋亡和ox-LDL减少的细胞粘附。最后，EGCG通过Jagged-1/Notch途径抑制载脂蛋白E（ApoE）敲除（ApoE-KO）小鼠中高脂饮食（HFD）诱导的动脉粥样硬化。综上所述，这些研究结果表明，50 µM EGCG通过Jagged-1/Notch信号通路保护ox-LDL诱导的内皮功能障碍。此外，我们的数据提供了对EGCG减轻ox-LDL诱导的血管内皮功能障碍的可能分子机制的深入了解。
Atherosclerosis is the most common cause of cardiovascular diseases worldwide. Oxidized low-density lipoprotein (ox-LDL) is a particularly important risk factor in the pathogenesis of atherosclerosis. Accumulating evidence has indicated that epigallocatechin-3-gallate (EGCG; a catechin found in the popular beverage, greent tea) protects against ox-LDL-induced atherosclerosis. However, the underlying mechanisms remain unclear. In the present study, ox-LDL (100 mg/l) induced damage to, and the apoptosis of human umbilical vein endothelial cells (HUVECs) by reducing endothelial nitric oxide synthase (eNOS) expression and promoting inducible nitric oxide synthase (iNOS) expression; these effects were abrogated by the addition of 50 µM EGCG. Furthermore, ox-LDL rapidly activated the membrane translocation of p22phox, and altered the protein expression of Jagged-1 and Notch pathway-related proteins [Math1, hairy and enhancer of split (HES)1 and HES5]; these effects were also prevented by pre-treatment with 50 µM EGCG. In addition, Jagged-1 played a significant role in the EGCG-mediated protection against ox-LDL-induced apoptosis and ox-LDL‑diminished cell adhesion in the HUVECs. Finally, EGCG inhibited high-fat diet (HFD)-induced atherosclerosis in apolipoprotein E (ApoE) knockout (ApoE-KO) mice through the Jagged-1/Notch pathway. Taken together, these findings demonstrate that 50 µM EGCG protects against ox-LDL-induced endothelial dysfunction through the Jagged-1/Notch signaling pathway. Moreover, our data provide insight into the possible molecular mechanisms through which EGCG attenuates ox-LDL‑induced vascular endothelial dysfunction.
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