缺血但不是药理学预条件要求蛋白质合成
N Matsuyama1, J E Leavens, D McKinnon
1Division of Cardiothoracic Surgery, The Institute for Molecular Cardiology, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.
Circulation
|November 18, 2000
概括
蛋白质合成对于缺血预先调节 (IPC) 心脏保护至关重要,它在转化层面起作用. 药理预制 (PPC) 可能涉及不同的机制,因为蛋白质合成抑制没有影响其保护作用.
科学领域:
- 心血管科学 心血管科学
- 分子心脏病学分子心脏病学
- 细胞生理学 细胞生理学
背景情况:
- 缺血预调 (IPC) 和药理预调 (PPC) 提供心脏保护.
- 蛋白质合成在这些先决条件机制中的确切作用仍然不清楚.
研究的目的:
- 研究蛋白质合成在IPC和PPC的心脏保护作用中的作用,无论是在转录和转化层面.
- 区分IPC和PPC背后的分子机制.
主要方法:
- 隔离的子心脏接受了由皮纳西迪尔 (一种对ATP敏感的通道开放剂) 诱导的IPC或PPC.
- 在预条件化之前,使用循环赫西米德 (翻译抑制剂) 或阿克丁诺米辛D (转录抑制剂) 抑制了蛋白质合成.
- 在经过一段时间的缺血和再输血后,测量了心脏病发作的大小,左心室压力,动作潜力的持续时间和冠状动脉流量.
主要成果:
- 与对照组相比,IPC和PPC都显著减少了心脏病发作的大小.
- 循环赫西米德的转化阻塞消除了IPC的心脏病限制作用,但没有PPC.
- 用actinomycin D进行转录封锁并没有影响IPC提供的心脏保护.
结论:
- 翻译层面的蛋白质合成在调解IPC的心脏保护作用方面发挥着至关重要的作用.
- IPC和PPC的保护机制似乎不同,IPC依赖于新的蛋白质合成.
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