叶酸可以防止酸甘诱导的氧化合成酶功能障碍和酸盐耐受性:一个人体体内实体研究
T Gori1, J M Burstein, S Ahmed
1Division of Cardiology, Department of Medicine, Mount Sinai Hospital, and the University of Toronto, Toronto, Canada.
Circulation
|September 6, 2001
概括
叶酸补充剂在健康志愿者中预防了尼甘诱导的内皮功能障碍和酸盐耐受性. 这表明四二氧化的生物可用性是氧化合成酶功能和酸盐耐受性的关键.
科学领域:
- 心血管药理学心血管药理学
- 内皮细胞功能 内皮细胞功能
- 氧化信号传输 氧化信号传输
背景情况:
- 持续的酸甘 (GTN) 治疗会损害氧化合成酶 (NOS) 功能,可能是由于四二烯 (BH4) 的生物可用性降低.
- 叶酸在各种疾病状态下与BH4再生有关.
- 叶酸在预防GTN诱导的NOS功能障碍和耐受性方面的作用需要研究.
研究的目的:
- 调查叶酸的使用是否能防止GTN诱导的NOS功能障碍.
- 为了确定叶酸补充是否可以防止对GTN.耐受性发展.
主要方法:
- 这是一项双盲,安慰剂控制的研究,涉及18名健康的男性志愿者.
- 参与者接受了口服叶酸 (10毫克/天) 或安慰剂一周,并连续通过皮肤GTN.
- 测量了前臂血液流动,使用plethysmography作为对血管活性剂的反应.
主要成果:
- 叶酸的使用防止了GTN诱导的内皮功能障碍,通过对乙胆和N-单甲基-L-氨酸的保留反应证明了这一点.
- 与安慰剂组相比,接受叶酸的受试者对静脉内GTN的反应显著增加.
- 叶酸补充剂减轻了酸盐耐受性.
结论:
- 补充叶酸有效地防止NOS功能障碍和酸盐耐受性,由健康个体持续GTN诱导.
- 降低BH4生物可用性被假设为这些现象的中心机制.
- 这些发现支持氧化应激在耐酸盐耐受性病原体中的作用.
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