Chromium chloride inhibits TNFα and IL-6 secretion in isolated human blood mononuclear cells exposed to high glucose
Chromium chloride inhibits TNFα and IL-6 secretion in isolated human blood mononuclear cells exposed to high glucose
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DOI：
10.1055/s-2006-924981
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发表时间：
2006-01-01
影响因子：
2.2
通讯作者：
Lim, G
中科院分区：
文献类型：
--
作者：
Jain, SK;Lim, G
血管炎症和心血管疾病（CVD）是糖尿病人群发病和死亡的主要原因，因此是一个重大的公共卫生问题[1, 2]。流行病学病例对照研究表明，脚趾甲中的铬 (Cr3+) 水平与一般人群中心肌梗死的风险之间存在负相关关系 [3]。同样，健康专业人员随访研究最近的一份报告发现，与健康对照组相比，患有糖尿病和心血管疾病的男性脚趾甲铬含量较低[4]。铬补充剂在一些国家很受欢迎[4]。 Cr3+ 对胰岛素敏感性和血管炎症产生影响的分子机制尚未研究。几种促炎细胞因子，包括肿瘤坏死因子α (TNFα) 和白细胞介素 (IL)−6，在许多炎症模型（包括糖尿病）中的血管并发症的发生中发挥着重要作用[2]。尚无研究检验铬对任何人类细胞中促炎细胞因子分泌的影响。这是第一项研究报告，补充 Cr3+ 可以阻止暴露于高葡萄糖浓度并从人类志愿者血液中分离的外周血单核细胞 (PBMC) 分泌 TNFα 和 IL−6。这为补充 Cr3+ 可以保护糖尿病患者免受血管炎症的新分子机制提供了证据。
Vascular inflammation and cardiovascular disease (CVD) are the leading causes of morbidity and mortality in the diabetic popula− tion, and are thus a major public health issue [1, 2]. Epidemiolog− ical case− control studies suggest an inverse association between chromium (Cr3+) levels in toenails and the risk of myocardial in− farction in the general population [3]. Similarly, a recent report within the Health Professionals Follow− up Study has found lower levels of toenail chromium among men with diabetes and CVD compared to healthy control subjects [4].Chromium supplementation is popular in some countries [4]. The molecular mechanisms by which Cr3+ produces its effects on insulin sensitivity and vascular inflammation have not yet been studied. Several pro− inflammatory cytokines, including tu− mor necrosis factor− alpha (TNFα) and interleukin (IL)− 6, play a significant role in the development of vascular complications in many models of inflammation, including diabetes [2]. No studies have examined the effect of chromium on secretion of pro− in− flammatory cytokines in any human cell. This is the first study to report that Cr3+ supplementation can prevent TNFα and IL− 6 secretion in exposed peripheral blood mononuclear cells (PBMC) exposed to high glucose concentrations and isolated from the blood of human volunteers. This provides evidence for a novel molecular mechanism by which Cr3+ supplementation may protect diabetic patients from vascular inflammation.