Vitamin E supplementation reduces plasma vascular cell adhesion molecule-1 and von Willebrand factor levels and increases nitric oxide concentrations in hypercholesterolemic patients
Vitamin E supplementation reduces plasma vascular cell adhesion molecule-1 and von Willebrand factor levels and increases nitric oxide concentrations in hypercholesterolemic patients
复制标题
DOI：
10.1210/jc.87.6.2940
复制
发表时间：
2002-06-01
影响因子：
5.8
通讯作者：
Ferri, C
中科院分区：
文献类型：
--
作者：
Desideri, G;Marinucci, MC;Ferri, C
血管细胞粘附分子-1 （VCAM-1）的上调和一氧化氮（NO）可用性的降低代表了动脉粥样硬化的早期特征。为了评估抗氧化剂维生素E是否影响高胆固醇血症患者循环中可溶性VCAM-1 （sVCAM-1）和血浆代谢产物NO（亚硝酸盐+硝酸盐）的水平，我们随机、双盲地给36例高胆固醇血症患者和22例年龄和性别匹配的对照组服用维生素E （400 IU或SW IU/d，持续8周）或安慰剂。在基线时，高胆固醇血症患者的血浆sVCAM-1（-1）高于对照组（591.2 +/- 132.5 vs. 505.0 +/- 65.6, P < 0.007）， NO代谢物（mu M）水平低于对照组（15.9 +/- 3.4 vs. 29.2 +/- 5.1, P < 0.0001）。在高胆固醇血症患者中，8周维生素E治疗显著降低循环sVCAM-1水平（400 IU:-148.9 +/ 84.6, P < 0.009; 800 IU:- 204.0 +/- 75.7, P < 0.0001；安慰剂：- 4.7 +/- 22.6，NS），而增加NO代谢物浓度（400 IU: +4.0 +/- 1.7, P < 0.02; 800 IU: +5.5 +/- 0.8, P < 0.0001；安慰剂：+0.1 +/- 1.1，NS），而不影响循环低密度脂蛋白水平。血浆sVCAM-1和NO代谢物水平的变化均与补充维生素E诱导的维生素E浓度变化呈显著相关（r = -0.515, P = 0.010; r = 0.435, P = 0.034）。综上所述，孤立的高胆固醇血症既增加了循环sVCAM-1，又降低了NO代谢物浓度。维生素E补充抵消了这些改变，因此代表了高胆固醇血症患者内皮保护的潜在工具。
Up-regulation of vascular cell adhesion molecule-1 (VCAM-1) and reduced nitric oxide (NO) availability represent early characteristics of atherosclerosis. To evaluate whether the antioxidant vitamin E affected the circulating levels of soluble VCAM-1 (sVCAM-1) and the plasma metabolite of NO (nitrite +nitrate) in hypercholesterolemic patients, either vitamin E (either 400 IU or SW IU/d for 8 wk) or placebo were randomly, double-blindly given to 36 hypercholesterolemic patients and 22 age- and sex-matched controls. At baseline hypercholesterolemic patients showed higher plasma sVCAM-1 (mug-liter(-1)) (591.2 +/- 132.5 vs. 505.0 +/- 65.6, P < 0.007) and lower NO metabolite (mu M) levels (15.9 +/- 3.4 vs. 29.2 +/- 5.1, P < 0.0001) than controls. In hypercholesterolemic patients, 8 wk vitamin E (but not placebo) treatment significantly decreased circulating sVCAM-1 levels (400 IU:-148.9 +/ 84.6, P < 0.009; 800 IU: -204.0 +/- 75.7, P < 0.0001; placebo: -4.7 +/- 22.6, NS), whereas it increased NO metabolite concentrations (400 IU: +4.0 +/- 1.7, P < 0.02; 800 IU: +5.5 +/- 0.8, P < 0.0001; placebo: +0.1 +/- 1.1, NS) without affecting circulating low-density lipoprotein levels. Changes in both plasma sVCAM-1 and NO metabolite levels showed a trend to significantly correlate (r = -0.515, P = 0.010; and r = 0.435, P = 0.034, respectively) with changes in vitamin E concentrations induced by vitamin E supplementation. In conclusion, isolated hypercholesterolemia both increased circulating sVCAM-1 and reduced NO metabolite concentrations. Vitamin E supplementation counteracts these alterations, thus representing a potential tool for endothelial protection in hypercholesterolemic patients.