Zinc supplementation decreases oxidative stress, incidence of infection, and generation of inflammatory cytokines in sickle cell disease patients
Zinc supplementation decreases oxidative stress, incidence of infection, and generation of inflammatory cytokines in sickle cell disease patients
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DOI：
10.1016/j.trsl.2008.06.001
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发表时间：
2008-08-01
影响因子：
7.8
通讯作者：
Swerdlow, Paul
中科院分区：
文献类型：
--
作者：
Bao, Bin;Prasad, Ananda S.;Swerdlow, Paul
锌缺乏在成人镰状细胞病（SCID）患者中很常见。我们以前证明，成人SCD患者补充锌可降低感染和住院率。我们假设补充锌可改善SCD患者T辅助细胞功能，降低血管内皮细胞活化、氧化应激和单核细胞（MNC）核因子-κ B（NF-κ B）-DNA结合。为了验证这一假设，招募了36名SCD患者，并随机分为2组。一组（n = 18）口服锌25毫克，每天三次，为期3个月。另一组（n 18）接受安慰剂。结果表明，与安慰剂组相比，锌补充组的感染发生率降低。补锌后，红细胞，血红蛋白（Hb），红细胞压积（Hct），血浆锌，和抗氧化能力增加;血浆亚硝酸盐和硝酸盐（NOx），脂质过氧化产物，DNA氧化产物，可溶性血管细胞粘附分子-1在补锌组，与安慰剂组相比，减少。与安慰剂组相比，锌补充患者表现出脂多糖诱导的肿瘤坏死因子-α（TNF-α）和IL-1 β mRNA以及TNF诱导的核因子κ β-DNA结合在MNC中显著降低。从安慰剂受试者分离的MNC中离体添加锌降低了TNF-α和IL-1 β mRNA。补锌也增加了植物血凝素-p刺激的MNC中IL-2和IL-2 R α mRNA的相对水平。这些结果表明，补锌可能对SCD患者有益。
Zinc deficiency is common in adult sickle-cell disease (SCID) patients. We previously demonstrated that zinc supplementation to adult SCD patients decreased the incidences of infections and hospital admissions. We hypothesize that zinc supplementation improves T-helper cell function and decreases vascular endothelial cell activation, oxidative stress, and nuclear factor-kappa B (NF-kappa B)-DNA binding in mononuclear cells (MNCs) in SCD patients. To test this hypothesis, 36 SCD patients were recruited and randomly divided into 2 groups. One group (n = 18) received 25-mg zinc orally thrice a day for 3 months. The other group (n 18) received placebo. The results indicate that the zinc-supplemented group had decreased incidence of infections compared with the placebo group. After zinc supplementation, red blood cell, hemoglobin (Hb), hematocrit, (Hct), plasma zinc, and antioxidant power increased; plasma nitrite and nitrate (NOx), lipid peroxidation products, DNA oxidation products, and soluble vascular cell adhesion molecule-1 decreased in the zinc-supplemented group, compared with the placebo group. Zinc-supplemented patients exhibited significant decreases in lipopolysaccharideinduced tumor necrosis factor-alpha (TNF-alpha) and IL-1 beta mRNAs, and TNF-induced nuclear factor Of kappa beta-DNA binding in MNCs, compared with the placebo group. Ex vivo addition of zinc to MNCs isolated from the placebo subjects decreased TNF-alpha, and IL-1 beta mRNAs. Zinc supplementation also increased relative levels of IL-2 and IL-2R alpha mRNAs in phytohemagglutinin-p-stimulated MNCs. These results suggest that zinc supplementation may be beneficial to SCD patients.