过高homocysteinemia通过氧化应激改变心脏基质代谢,通过氧化应激损害氧化的生物利用性
Nobuhiro Suematsu1, Caroline Ojaimi, Shintaro Kinugawa
1Department of Physiology, New York Medical College, Valhalla, NY 10595, USA.
Circulation
|January 4, 2007
概括
超同胞蛋白血症 (HHcy) 通过增加氧化应激和改变心肌代谢,损害心脏功能. 亚酸和其他抗氧化剂可以恢复正常的心脏功能,这表明了相关心脏病的新治疗点.
科学领域:
- 心血管生理学心血管生理学
- 代谢研究研究 代谢研究
- 氧化压力生物学 氧化压力生物学
背景情况:
- 超同胞蛋白血症 (HHcy) 与血管疾病和氧化压力有关.
- HHcy对心脏功能和心肌代谢的特定影响仍然基本上未被描述.
研究的目的:
- 在狗模型中研究HHcy对心脏功能,NO生物可用性和心肌基质利用的影响.
- 探索氧化应激在HHcy诱导的心脏改变中的作用.
主要方法:
- 静脉注射L-homocysteine和食氨酸以诱导意识犬的急性和慢性HHcy.
- 血液动力学,NO依赖冠状动脉扩张和心肌基质吸收 (葡萄糖,乳酸,自由脂肪酸) 的评估.
- 关于心肌氧消耗的体外研究和关键蛋白质 (Nox2, eNOS, SOD-1) 的西方斑点分析.
主要成果:
- HHcy没有显著改变血液动力学,但减少了依赖NO的血管扩张,这种扩张被抗氧化剂恢复.
- 心脏葡萄糖和乳酸摄取量增加,而自由脂肪酸摄取量在HHcy.下降.
- HHcy降低了心肌的氧气消耗,这种效应被抗氧化剂逆转,并增加了Nox2,同时降低了eNOS和SOD-1表达.
结论:
- HHcy通过超氧化物生成减少NO的生物可用性,独立于血液动力学变化,直接改变心脏基质利用和新陈代谢.
- 这些发现突显了氧化应激在与HHcy相关的心脏功能障碍中的关键作用,并建议评估心脏代谢变化的疾病进展.
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