Reduction of oxidative stress by oral N-acetyl-L-cysteine treatment decreases plasma soluble vascular cell adhesion molecule-1 concentrations in non-obese, non-dyslipidaemic, normotensive, patients with non-insulin-dependent diabetes
Reduction of oxidative stress by oral N-acetyl-L-cysteine treatment decreases plasma soluble vascular cell adhesion molecule-1 concentrations in non-obese, non-dyslipidaemic, normotensive, patients with non-insulin-dependent diabetes
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DOI：
10.1007/s001250051082
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发表时间：
1998-11-01
期刊：
影响因子：
8.2
通讯作者：
Ferri, C
中科院分区：
文献类型：
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作者：
De Mattia, G;Bravi, MC;Ferri, C
为探讨抗氧化剂对血管细胞黏附分子-1表达的影响，对无并发症的非胰岛素依赖型糖尿病患者(男性9例，女性6例，年龄48+/-6岁)随机、交叉、双盲口服N-乙酰-L半胱氨酸(1.200 mg/d)或安慰剂治疗1个月后，测定其血中可溶性血管细胞黏附分子-1、红细胞内还原型谷胱甘肽和还原型谷胱甘肽的浓度。10例健康受试者(男7例，女3例，年龄52+/-3岁)为对照组。非胰岛素依赖型糖尿病患者基础血浆血管细胞黏附分子-1浓度(707.9±52.5 ng/ml)高于对照组(627.3±84.6 ng/ml)(P=0.007)。非胰岛素依赖型糖尿病患者红细胞内GSSG含量(0.618+/-0.185 mU/g Hb)高于对照组(0.352+/-0.04mU/g Hb，P=0.0002)，而非胰岛素依赖型糖尿病患者红细胞内GSH含量(6.0/-0.7mU/g Hb)低于对照组(7.1+/-0.5 mU/g Ib，P=0.001)。第一组平均GSH/GSSG比值(10.9+/-4.5)也低于第二组(20.2+/-1.4)(P=0.0001)。在非胰岛素糖尿病患者中，循环血管细胞黏附分子-1与红细胞内CSI-I浓度呈负相关(r=0.605，P=0.01)。非胰岛素依赖型糖尿病患者经N-乙酰半胱氨酸治疗后，血浆血管细胞间黏附分子-1和红细胞内谷胱甘肽水平显著降低(p=0.006)，谷胱甘肽浓度和谷胱甘肽/谷胱甘肽比值显著升高(p=0.004)。我们的数据表明，非胰岛素依赖型糖尿病患者血管内皮细胞被激活。抗氧化剂治疗抵消了这种内皮细胞的激活。因此，抗氧化剂可能防止氧化剂相关的内皮细胞黏附分子上调，并减缓非胰岛素依赖型糖尿病血管损伤的进展。
To assess in vivo effects of antioxidants on vascular cell adhesion molecule (VCAM)-1 expression, circulating soluble VCAM-1 and intraerythrocytic reduced glutathione (GSH) and GSH disulphide (GSSG) concentrations were evaluated in non-insulin-dependent diabetic patients without complications (9 men, 6 women, 48 +/- 6 years old) before and after 1 month of either oral N-acetyl-L-cysteine (1.200 mg/day) or placebo treatments, given in randomized, cross-over, double-blind fashion. Ten healthy subjects (7 men, 3 women, 52 +/- 3 years old) served as control subjects. Baseline plasma VCAM-1 concentrations were higher (p = 0.007) in non-insulin-dependent diabetic patients (707.9 +/- 52.5 ng/ml) than in control subjects (627.3 +/- 84.6 ng/ml). Intraerythrocytic GSSG content was higher (non-insulin dependent diabetic patients: 0.618 +/- 0.185 mu mol/g Hb; control subjects: 0.352 +/- 0.04 mu mol/g Hb, p = 0.0002), whereas intraerythrocytic GSH concentrations were lower (p = 0.001) in non-insulin dependent diabetic patients (6.0 +/- 0.7 mu mol/g Hb) than in control subjects (7.1 +/- 0.5 mu mol/g Ib). The mean GSH:GSSG ratio was also lower (p = 0.0001) in the first (10.9 +/- 4.5) than in the second group (20.2 +/- 1.4). Circulating VCAM-1 and intraerythrocytic CSI-I concentrations were negatively correlated in non-insulin diabetic patients (r = 0.605, p = 0.01). Treatment with N-acetyl-L-cysteine decreased plasma VCAM-1 (p = 0.01) and intraerythrocytic GSSG (p = 0.006) but increased GSH concentrations (p = 0.04) and the GSH:GSSG ratio (p = 0.004) in non-insulin dependent diabetic patients. Our data indicate that the vascular endothelium is activated in non-insulin dependent diabetes. Antioxidant treatment counterbalanced such endothelial activation. Thus, antioxidant agents might protect against oxidant-related upregulation of endothelial adhesion molecules and slow down the progression of vascular damage in non-insulin dependent diabetes.