Antioxidant supplementation with or without B-group vitamins after acute ischemic stroke: A randomized controlled trial

Antioxidant supplementation with or without B-group vitamins after acute ischemic stroke: A randomized controlled trial
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DOI:
10.1177/0148607106030002108
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发表时间:
2006-03-01
影响因子:
3.4
通讯作者:
Gariballa, Salah E.
Gariballa, Salah E.
中科院分区:
医学3区
文献类型:
--
作者:
Ullegaddi, Rajesh;Powers, Hilary J.;Gariballa, Salah E.

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背景资料:有证据表明,急性缺血性卒中后氧化损伤标志物的产生迅速增加,内源性抗氧化防御迅速耗尽,从而允许进一步的组织损伤。一些研究指出B族维生素的抗氧化作用和血浆总同型半胱氨酸(tHcy)升高的促氧化作用。研究方法:为了测试在这一关键时期补充抗氧化剂(含或不含B族维生素)是否能增强抗氧化能力或减轻氧化损伤,96名症状发作12小时内的急性缺血性卒中患者被随机分配接受每日口服800 IU(727 mg)维生素E和500 mg维生素C(n = 24)或B族维生素(5毫克叶酸、5毫克维生素B-2、50毫克维生素B-6和0.4克维生素B-12; n = 24)、两种维生素一起(n = 24)或不补充(n = 24)14天。治疗组和对照组的中风亚型和年龄相匹配。在治疗前、第71天和第14天采集血液,用于测量血浆或血液维生素状态、血浆总抗氧化能力(TAOC)、丙二醛(MDA)、tHcy和C-反应蛋白(CRP)。结果如下:与对照组相比,单独或同时补充抗氧化维生素和B族维生素显著增加了维生素C、E、磷酸吡哆醛(B-6状态)、红细胞叶酸的血浆浓度,并改善了B-2状态(红细胞谷胱甘肽还原酶活化系数[EGRAC])。与对照组中观察到的非显著性下降相比,抗氧化剂治疗组中的血浆TAOC显著增加。与仅接受抗氧化剂的受试者相比,接受B族维生素和对照组的tHcy浓度下降。有一个显着的减少,在3个治疗组的血浆MDA浓度,在对照组中看到的增加相反,但是,变化是最明显的抗氧化剂组。CRP浓度(组织炎症的标志物)在3组中显著较低。治疗组与对照组比较。抗氧化剂和B族维生素在任何结果测量上都没有相加或协同作用。结论:抗氧化剂补充或不补充B族维生素可增强抗氧化能力,减轻氧化损伤,并可能在卒中后立即产生抗炎作用。
Background: Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately after acute ischemic stroke and that endogenous antioxidant defenses are rapidly depleted, thus permitting further tissue damage. Several studies point to an antioxidant effect of B-group vitamins and a pro-oxidant effect of elevated total plasma homocysteine (tHcy). Methods: To test whether supplementary antioxidants with or without B-group vitamins during this critical period enhance antioxidant capacity or mitigate oxidative damage, ninety-six acute ischemic stroke patients within 12 hours of symptom onset were randomly assigned to receive either daily oral 800 IU(727 mg) vitamin E and 500 mg vitamin C (n = 24), or B-group vitamins (5 mg folic acid, 5 mg vitamin B-2, 50 mg vitamin B-6 and 0.4 in g of vitamin B-12; n = 24), both vitamins together (n 24), or no supplementation (n = 24) for 14 days. Treatment groups and controls were matched for stroke subtype and age. Blood was obtained before treatment, at day 71 and day 14 for measurements of plasma or blood vitamin status, plasma total antioxidant capacity (TAOC) malondialdehyde (MDA), tHcy and C-reactive protein (CRP). Results: Supplementation with antioxidant vitamins and B-group vitamins separately or together significantly increased the plasma concentration of vitamin C, E, pyridoxal phosphate (B-6 status), red blood cell folate, and improved a measure of B-2 status (red cell glutathione reductase activation coefficient [EGRAC]) compared with the control group. Plasma TAOC increased significantly in the antioxidant treatment groups compared with the nonsignificant decline seen in the control group. tHcy concentrations decreased in subjects who received B-group vitamins and the control group compared with the rise seen in those who received antioxidants alone. There was a significant reduction in plasma MDA concentration in the 3 treatment groups, in contrast to the increase seen in the control,group; however, the changes were most evident in antioxidant groups. CRP concentrations (a marker of tissue inflammation) were significantly lower in the 3. treatment groups compared with the control group. There were no additive or synergistic effects of antioxidants and B-group vitamins together on any outcome measure. Conclusions: Antioxidants supplementation with or without B-group vitamins enhances antioxidant capacity, mitigates oxidative damage, and may have an anti-inflammatory effect immediately postinfarct in stroke disease.