Departamento de Farmacia de la Facultad de Química, Universidad Autónoma del Estado de México (UAEMex), Toluca, Mexico.
Am J Ther. 2013 Jul-Aug;20(4):422-31. doi: 10.1097/MJT.0b013e318235f32f.
Cardiovascular disease is originated in the vascular endothelium, which controls the homeostasis and the filtration and diffusion of molecules from blood to the tissues. The classical cardiovascular risk factors (CRFs) act directly on the endothelium through an increase in the production of reactive oxygen species, promoting an endothelial activation mediated by the expression of adhesion and proinflammatory molecules, which lead to endothelial dysfunction, the progression of the atherosclerotic plaque, and the onset of cardiovascular disease. The objective of this study was to analyze the association of superoxide dismutase, catalase, gluthatione peroxidase, and lipoperoxidation with fibrinogen, interleukin (IL)-6, tumor necrosis factor-α, and vascular cell adhesion molecule (VCAM)-1 in subjects with cardiovascular risk (CVR) and CRF. This was a cross-sectional study of 114 individuals; oxidative stress (superoxide dismutase, catalase, gluthatione peroxidase, and lipoperoxidation) and inflammatory (fibrinogen, IL-6, tumor necrosis factor-α, and VCAM-1) biomarkers were measured; a CVR score (Framingham) and its CRF were taken into consideration to classify the participants. Twenty-nine subjects out of a total of 114 had high CVR. Smokers and subjects with diabetes (43 subjects) were excluded from the low CVR group. Significant decreases in lipoperoxidation, IL-6, and VCAM-1 and an increase in SOD were found in the high CVR group (P ≤ 0.05). Individual analysis of each CRF in the 114 subjects revealed a different pattern in the biomarkers' statistical differences. Concluding that the biomarkers show statistical differences in each CRF, especially IL-6, VCAM-1, and SOD; therefore, these are highly recommended to be used as biomarkers of the oxidative stress and inflammatory status in CVR.
心血管疾病起源于血管内皮细胞,它控制着血液与组织之间的分子的内稳态和过滤扩散。经典的心血管危险因素(CRF)通过增加活性氧的产生直接作用于内皮细胞,促进由粘附和促炎分子表达介导的内皮激活,从而导致内皮功能障碍、动脉粥样硬化斑块的进展和心血管疾病的发生。本研究的目的是分析超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和脂质过氧化与纤维蛋白原、白细胞介素(IL)-6、肿瘤坏死因子-α和血管细胞黏附分子(VCAM)-1在具有心血管风险(CVR)和 CRF 的个体中的相关性。这是一项横断面研究,共纳入 114 名个体;测量了氧化应激(超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和脂质过氧化)和炎症(纤维蛋白原、IL-6、肿瘤坏死因子-α和 VCAM-1)生物标志物;考虑了 CVR 评分(Framingham)及其 CRF,对参与者进行分类。在总共 114 名参与者中,有 29 名患有高 CVR。将吸烟者和患有糖尿病的受试者(43 名)排除在低 CVR 组之外。在高 CVR 组中,脂质过氧化、IL-6 和 VCAM-1 显著降低,SOD 升高(P≤0.05)。对 114 名受试者的每个 CRF 进行个体分析,发现生物标志物的统计差异存在不同模式。结论是,在每个 CRF 中,生物标志物显示出统计学差异,特别是 IL-6、VCAM-1 和 SOD;因此,强烈推荐将其作为 CVR 中氧化应激和炎症状态的生物标志物。