腺氨酸A(1) 受体的激活会诱导由超氧化物失调酶介导的老鼠延迟预条件
A Dana1, A K Jonassen, N Yamashita
1Hatter Institute and Centre for Cardiology, University College London Hospitals and Medical School, London, UK.
Circulation
|June 22, 2000
概括
腺氨酸A(1) 受体的激活在老鼠中触发了延迟的心脏保护. 这种保护是由抗氧化酶 - - 线粒体超氧化脱酶 (Mn-SOD) 的增加介导的.
科学领域:
- 心血管研究研究心血管研究
- 线粒体生物学 线粒体生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 在腺A(1) 受体激活后,在子中观察到延迟的心脏保护.
- 研究了线粒体超氧化物脱酶 (Mn-SOD) 在调解这种保护中的作用.
研究的目的:
- 为了确定腺A(1) 受体 (A(1) R) 的激活是否会在老鼠中诱导延迟的心脏保护.
- 阐明线粒体Mn-SOD在这种保护作用中的作用.
主要方法:
- 小鼠接受了A(1) R激动剂CCPA或盐水,有或没有Mn-SOD反感 oligodeoxynucleotide (ODN).
- 在治疗后24小时内,心脏经历了区域性缺血和再输血.
- 评估了心脏梗塞的大小,心肌的Mn-SOD含量和活动.
主要成果:
- 与对照组相比,CCPA显著减少了心脏病发作的大小 (22.3%与42.1%相比).
- 反感ODN取消了CCPA诱导的心脏保护.
- CCPA增加了心肌的Mn-SOD含量和活性,这种效果被反感性ODN阻止.
结论:
- 暂时的A(1) R激活会在老鼠中诱导延迟的心脏保护.
- 线粒体Mn-SOD在这种延迟保护中发挥着关键作用,作为终端效应因子.
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