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抗体可以通过抑制蛋白激酶C来改善缺血诱导的内皮细胞透性
A Hempel1, C Lindschau, C Maasch
1Franz Volhard Clinic, Humboldt University of Berlin, Germany.
Circulation
|May 20, 1999
概括
尼菲迪平通过抑制蛋白激酶C (PKC),独立于通道,防止缺血引起的内皮细胞通透性的增加. 这表明二皮里丁抗体可能通过它们对内皮细胞的作用,部分保护免受缺血.
科学领域:
- 内皮细胞生物学 内皮细胞生物学
- 心血管研究的心血管研究.
- 药理学 药理学是指药理学的学科.
背景情况:
- 二皮里丁是众所周知的通道阻断剂.
- 缺少通道的内皮细胞也受到二二的影响.
- 这项研究调查了尼费迪平通过蛋白激酶C (PKC) 对内皮通透性的影响.
研究的目的:
- 测试尼菲迪平能否防止缺血引起的内皮膜通透性增加.
- 要确定这种效应是否通过抑制蛋白激酶C (PKC) 来实现.
- 探索特定PKC异型体在内皮细胞透性中的作用.
主要方法:
- 在培养的猪内皮细胞中使用化/脱氧葡萄糖诱导缺血症.
- 测量蛋白流量的透性,细胞内 ([Ca2+]i) 与fura 2,以及PKC活性.
- 评估PKC异形转位使用西斑和共聚焦显微镜.
主要成果:
- 尼菲迪平剂量依赖地预防了缺血引起的透性增加.
- 缺血诱导的PKC转位,但没有增加[Ca2+]i,被尼菲迪平抑制.
- 尼菲迪平阻止了PKC-alpha和PKC-zeta的转位;PKC-alpha的抑制是至关重要的.
结论:
- 尼菲迪平直接影响内皮细胞的透性,独立于通道.
- 尼菲迪平抑制缺血引起的透性主要通过抑制PKC-alpha.
- 狄皮里丁抗体可能通过调节内皮细胞透性来提供抗缺血益处.
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