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首页> 美国卫生研究院文献>other >Ginkgolide B Reduces LOX-1 Expression by Inhibiting Akt Phosphorylation and Increasing Sirt1 Expression in Oxidized LDL-Stimulated Human Umbilical Vein Endothelial Cells
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Ginkgolide B Reduces LOX-1 Expression by Inhibiting Akt Phosphorylation and Increasing Sirt1 Expression in Oxidized LDL-Stimulated Human Umbilical Vein Endothelial Cells

机译：银杏内酯B通过抑制Akt磷酸化并增加氧化LDL刺激的人脐静脉内皮细胞中Sirt1的表达来降低LOX-1的表达。

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Oxidized low-density lipoprotein (ox-LDL) is an important risk factor in the development of atherosclerosis. LOX-1, a lectin-like receptor for ox-LDL, is present primarily on endothelial cells and upregulated by ox-LDL, tumor necrosis factor a, shear stress, and cytokines in atherosclerosis. Recent studies demonstrated that ginkgolide B, a platelet-activating factor receptor antagonist, has antiinflammatory and antioxidant effects on endothelial and nerve cells. The present study investigated the effects of ginkgolide B on LOX-1 expression and the possible mechanism of action. Our results showed that ginkgolide B inhibited LOX-1 and intercellular cell adhesion molecule-1 (ICAM-1) expression in ox-LDL-stimulated endothelial cells through a mechanism associated with the attenuation of Akt activation. Similar data were obtained by silencing Akt and . We also evaluated Sirt1 and nuclear factor erythroid 2-related factor 2 (Nrf2) expression. These molecules play a protective role in endothelial cell injury. The results showed that ginkgolide B increased Sirt1 expression in ox-LDL-treated cells. The inhibitory effects of ginkgolide B on LOX-1 and ICAM-1 expression were reduced in Sirt1 siRNA-transfected cells. Nrf2 expression was increased in ox-LDL-treated cells, and ginkgolide B downregulated Nrf2 expression. These results suggest that ginkgolide B reduces Nrf2 expression by inhibiting LOX-1 expression, consequently reducing oxidative stress injury in ox-LDL-stimulated cells. Altogether, these results indicate that the protective effect of ginkgolide B on endothelial cells may be attributable to a decrease in LOX-1 expression and an increase in Sirt1 expression in ox-LDL-stimulated endothelial cells, the mechanism of which is linked to the inhibition of Akt activation. Ginkgolide B may be a multiple-target drug that exerts protective effects in ox-LDL-treated human umbilical vein endothelial cells.
机译：氧化的低密度脂蛋白（ox-LDL）是动脉粥样硬化发展的重要危险因素。 LOX-1是ox-LDL的一种凝集素样受体，主要存在于内皮细胞上，并由ox-LDL，肿瘤坏死因子a，剪切应力和动脉粥样硬化中的细胞因子上调。最近的研究表明，血小板活化因子受体拮抗剂银杏内酯B对内皮细胞和神经细胞具有抗炎和抗氧化作用。本研究调查了银杏内酯B对LOX-1表达的影响及其可能的作用机制。我们的结果表明，银杏内酯B通过与Akt激活减弱相关的机制抑制ox-LDL刺激的内皮细胞中的LOX-1和细胞间细胞粘附分子1（ICAM-1）表达。通过使Akt和Akt沉默获得相似的数据。我们还评估了Sirt1和核因子红系2相关因子2（Nrf2）的表达。这些分子在内皮细胞损伤中起保护作用。结果表明，银杏内酯B可增加经ox-LDL处理的细胞中Sirt1的表达。在Sirt1 siRNA转染的细胞中，银杏内酯B对LOX-1和ICAM-1表达的抑制作用降低。在ox-LDL处理的细胞中Nrf2表达增加，银杏内酯B下调Nrf2表达。这些结果表明银杏内酯B通过抑制LOX-1的表达降低Nrf2的表达，从而减少ox-LDL刺激的细胞的氧化应激损伤。总之，这些结果表明银杏内酯B对内皮细胞的保护作用可能归因于ox-LDL刺激的内皮细胞中LOX-1表达的减少和Sirt1表达的增加，其机制与抑制作用有关。 Akt激活。银杏内酯B可能是在ox-LDL处理的人脐静脉内皮细胞中发挥保护作用的多靶点药物。

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