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伊尔贝萨坦但不是阿姆洛迪平抑制了与糖尿病相关的动脉样硬化
Riccardo Candido1, Terri J Allen, Markus Lassila
1Vascular Division, Baker Heart Research Institute, PO Box 6492, Melbourne 8008, Victoria, Australia.
Circulation
|March 17, 2004
概括
血管新素II亚型1受体阻塞与伊尔贝萨坦,但不是安洛迪平,降低了糖尿病小鼠的动脉样硬化. 这表明氨酸 - 血管素系统在糖尿病加速血管疾病中起着关键作用.
科学领域:
- 心血管研究研究心血管研究
- 药理学 药理学是指药理学的学科.
- 糖尿病是一种糖尿病.
背景情况:
- 氨酸-血管增生素系统 (RAS) 阻断在减轻糖尿病患者动脉样硬化的作用仍在争论中.
- 将RAS抑制剂与其他抗高血压药物的比较对于了解糖尿病中心血管保护至关重要.
研究的目的:
- 在糖尿病小鼠模型中,比较伊尔贝萨坦 (AT1受体阻塞剂) 和安洛迪平 (通道抗剂) 的抗动脉样硬化作用.
- 研究糖尿病诱导动脉样硬化中血管保护的基础分子机制.
主要方法:
- 在阿波利波蛋白E-null小鼠中,使用链毒素使它们变得糖尿病.
- 糖尿病小鼠在20周内没有接受治疗,也没有接受伊尔贝沙坦或阿姆洛迪平的治疗.
- 评估了大动脉斑块的形成,受体表达,细胞透和炎症标志物.
主要成果:
- 糖尿病增加了大动脉斑块面积,复杂性和AT1受体,PDGF-B,MCP-1和VCAM-1的表达.
- 伊尔贝萨坦显著减轻了动脉样硬化发展和相关的分子变化.
- 尽管可以比较降低血压,阿姆洛迪平并没有显示出显著的抗动脉样硬化作用.
结论:
- 阻断AT1受体有效地改善了与糖尿病相关的动脉样硬化.
- 通道对抗性并没有提供类似的血管保护.
- 这些发现强调了血管RAS在糖尿病驱动动的动脉样硬化进展中的关键作用.
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