缺氧对血管内皮生长因子诱导主动脉内皮细胞通透性增加的调控研究
Hypoxia regulate vascular endothelial growth factor-induced hyperpermeability in bovine artery endothelial cell
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摘要: 目的 为了解缺氧对血管内皮生长因子(VEGF)增强血管内皮细胞通透性作用的影响,考察正常和缺氧状态下VEGF对体外培养牛主动脉内皮细胞(BAEC)脂蛋白通透性的影响及银杏叶提取物(Egb761)的抑制作用。方法 将VEGF及Egb761加入BAEC共孵育,用SN-695型液闪计数器测[125I]氧化低密度脂蛋白([125I]OxLDL)通过BAEC的百分率。结果 VEGF可显著增强BAEC对[125I]OxLDL的通透性(P<0.01),这种增加具有浓度依赖性。缺氧3h可促进VEGF所致的的通透性增加。Egb761能显著抑制VEGF诱导的通透性升高(P<0.01)。结论 VEGF在动脉粥样硬化的形成和发展过程中起一定作用。Egb761对VEGF诱导血管内皮通透性升高有显著的抑制作用。Abstract: Objective In order to understand the regulation of hypoxia on the vascular endothelial growth factor (VEGF) permeability action, particularly in relation to the risk of development of atherosclerosis, the effect of recombinant human VEGF on the oxidation low density lipoprotein (OxLDL) permeability of bovine aortic endothelial cells (BAEC) was observed under the hypoxia condition in vitro.Methods Under normal or hypoxia condition, the confluence BAEC monolayers were cultured with normal medium and with medium containing VEGF at various concentrations and for various time periods. The Iodine labeled low density lipoprotein flux across the monolayers was then performed, and the radioactivity was measured by SN 695 automatic liquid scintillation counter. Results Addition of VEGF to the BAEC monolayers significantly increased the permeability of the monolayer to [125I]OxLDL (P<0.01). The permeability increasing activity of VEGF on the BAEC monolayers was concentration dependent. Hypoxia injury on endothelial cells increased VEGF induced hyperpermeability. Conclusion VEGF plays a role in the formation and development of atherosclerosis.
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Key words:
- hypoxia /
- vascular endothelial /
- growth substances /
- permeability
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