动脉样硬化的回归:氧化和亡的作用
1Section of Vascular Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, Calif, USA.
Circulation
|March 9, 1999
概括
补充L-氨酸通过增加氧化 (NO) 水平,诱导动脉样硬化病变中的巨细胞的亡. 这表明通过操纵NO合成酶通路来治疗动脉样硬化的潜在治疗策略.
科学领域:
- 心血管研究研究心血管研究
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 在高胆固醇贫血的子中,L-氨酸的使用促进了动脉样硬化病变的回归.
- 氧化 (NO) 合成酶通路的激活可以在体外诱导血管细胞亡.
研究的目的:
- 为了确定饮食中的L-氨酸补充剂是否会在亲密的动脉样硬化病变中诱导亡.
- 为了调查这种亡效应是否由NO合成酶途径介导.
主要方法:
- 患有高胆固醇血症的子被食胆固醇饮食,并补充L-氨酸.
- 大动脉细分被用NO合成途径调节器进行了ex vivo分析.
- 从组织学上评估了亡,并测量了氧化.
主要成果:
- 在内脏病变中,L-氨酸治疗增加了三倍的亡细胞 (主要是巨细胞).
- 酸和L-氨酸增加了细胞亡和氧化的释放.
- 这些效应被NO合成酶抑制剂对抗,而不是D-arginine模仿.
结论:
- 补充L-氨酸通过通过cGMP独立的途径通过NO生产诱导动脉样硬化病变中的巨细胞亡.
- 这些发现支持先前关于L-氨酸在动脉瘤回归中的作用的观察.
- 这项研究为在动脉样硬化治疗中探索NO合成途径操纵提供了理由.
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