氧化应激和肿瘤坏死因子- α、丙二醛和铁在高血压中降低抗氧化能力的生物标志物

M. Verma, A. Jaiswal, Preeti Sharma, Pradeep Kumar, A. Singh
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引用次数: 0

摘要

背景:伴随着氧化剂和抗氧化剂的失衡,高血压(BP)是当前情况下主要的身体状况负担。肿瘤坏死因子α (Tumor necrosis factor -α, TNF-α)在高血压(HTN)的发病过程中起着至关重要的作用。TNF-α抑制剂改善临床症状;然而,他们对高血压的结果尚未调查。我们研究了高血压患者的炎症标志物TNF-α、丙二醛(MDA)和铁还原抗氧化能力(FRAP)。我们在高血压患者中使用动态观察随机测量血压。收缩压140mmhg和/或舒张压90mmhg被认为是高血压。材料与方法:本研究共纳入60例高血压患者30例,正常对照30例(30)。两组均检测HTN患者血清TNF-α、MDA和FRAP浓度。结果:与正常组相比,研究对象血清TNF-α明显升高(r = 0.32,P < 0.0001*)。与正常对照组相比,高血压组血清MDA升高(r = 0.99**,P < 0.0001*),而高血压组血清FRAP降低(r = 0.23,P < 0.0001*)。结论:高BP可导致氧化应激的产生,TNF-α和MDA水平显著升高。提示铁还原抗氧化能力(FRAP)水平降低,提示氧化应激在高血压病理生理中的可能作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxidative stress and biomarker of tumor necrosis factor-alpha, malondialdehyde, and ferric reducing antioxidant power in hypertension
Background: Concurrent with the imbalance of oxidizing agents and antioxidants, high blood pressure (BP) is a major physical condition burden in the current scenario. Tumor necrosis factor-alpha (TNF-α) plays a vital role in the pathogenesis of hypertension (HTN). TNF-α inhibitor improves clinical symptoms; however, their outcome on high BP has not been investigated. We investigated the inflammatory marker TNF-α, malondialdehyde (MDA), and ferric reducing antioxidant power (FRAP) in hypertensive patients. We measured BP randomly using an ambulatory observe in hypertensive patients. Measured systolic BP was 140 mmHg and/or diastolic BP was 90 mmHg were considered hypertensive. Materials and Methods: A total of 60 cases were considered in the study involving 30 hypertensive patients and 30 normal controls (30). Measurements of serum concentrations of TNF-α, MDA, and FRAP in HTN patients were done in both the groups. Results: Serum TNF-α was found to be remarkably increased in study participants as compared to the normal group (r = 0.32,P < 0.0001*). Serum MDA was also raised in hypertensive as compared to the control group (r = 0.99**,P < 0.0001*), whereas serum FRAP was found to be decreased in the hypertensive group in comparison to the healthy controls (r = 0.23,P < 0.0001*). Conclusions: It is concluded that high BP leads to the generation of oxidative stress with a remarkable elevation of TNF-α and MDA levels. The indicates decrease level of Ferric Reducing Antioxidant Power (FRAP) and suggest a possible role of oxidative stress in the pathophysiology of hypertension.
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