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Analytical Techniques for Assaying Nitric Oxide Bioactivity
Published on: June 18, 2012
酸甘油未能降低 redox-dead Cys42Ser PKG1α 敲进小鼠中的血压
Olena Rudyk1, Oleksandra Prysyazhna, Joseph R Burgoyne
1Cardiovascular Division, King's College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St. Thomas' Hospital, United Kingdom.
Circulation
|June 12, 2012
概括
酸甘油是一种酸甘油.
科学领域:
- 心血管药理学心血管药理学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 亚甘油降低血压的机制尚未完全理解.
- 酸甘油生物激活产生氧化剂对于血管扩张至关重要.
- 蛋白激酶G 1α (PKG1α) 可以通过氧化通过二硫化物形成来激活.
研究的目的:
- 为了研究是否尼特甘氨酸诱导的血管扩张是由PKG1α的二硫化激活介导的.
- 为了探索PKG1α氧化在尼甘耐受性中的作用.
主要方法:
- 评估了PKG1α二硫化二分化在平滑肌肉细胞和用酸甘治疗的分离血管中.
- 在活体中酸甘给药后,在小鼠大动脉中检查了PKG1α氧化.
- 利用Cys42Ser PKG1α敲入小鼠模型来评估氧化还原感应硫醇对尼甘氨酸低血压效应和血管扩张的必要性.
- 在野生类型和敲进小鼠中测量了体内血压反应和体外血管对酸甘油的敏感性.
主要成果:
- 甘治疗诱导了PKG1α二硫化物二重化在体外和体内.
- 随着野生类型小鼠对酸甘的耐受性发展,PKG1α氧化减少.
- 在Redox-dead的PKG1α敲门小鼠中,显著减少了对酸甘的低血压反应.
- 试验小鼠对尼甘诱导的血管扩张敏感性降低,缺乏耐受性发展.
结论:
- 形成PKG1α二硫化物是尼特甘氨酸诱导血管扩张的关键媒介.
- 氧化PKG1α的损失与耐酸盐耐受性的发展有关.
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