Center for Integrated Research, Department of Laboratory Medicine and Microbiology, Campus Bio-Medico, University of Rome, Italy.
Dis Markers. 2013;35(3):141-7. doi: 10.1155/2013/246205. Epub 2013 Aug 20.
Sulfhydryl groups (SH) are considered a key factor in redox sensitive reaction of plasma, and their modification could be considered an expression of abnormal generation of oxygen free radicals.
Fifty consecutive patients with acute brain stroke were enclosed in this study. The plasma concentrations of SH groups were correlated to cytokines (IL-1b, IL-6, IL-8, TNF- α ), plasma chitotriosidase (Chit), metalloprotease (MMP2-9), intercellular adhesion molecule-1 (ICAM-1).
The results demonstrated a significant reduction of SH groups within 24 hours from the onset of an acute ischemic stroke, a reduction of plasma IL-1b, IL-6, and IL-8, and an increase of Chit and TNF- α in relation to the stroke severity.
The observation of an intense microenvironment activation that follows the stroke and the correlation between SH levels and markers of immune response suggest that, especially in stroke, is necessary to maintain the redox function to prevent the brain damage. The reduced SH levels represent an attempt to neutralize the abnormal generation of free radicals. Since the reperfusion of brain after ischemic event represents a severe oxidative stress, which must be corrected by regeneration of redox sensitive function, pharmacological intervention could be beneficial in this setting.
巯基(SH)被认为是血浆中氧化还原敏感反应的关键因素,其修饰可以被认为是氧自由基异常生成的表达。
本研究纳入了 50 例连续的急性脑卒患者。将 SH 组的血浆浓度与细胞因子(IL-1b、IL-6、IL-8、TNF-α)、血浆壳聚糖酶(Chit)、金属蛋白酶(MMP2-9)、细胞间黏附分子-1(ICAM-1)相关联。
结果表明,急性缺血性脑卒中发病后 24 小时内 SH 组显著减少,血浆 IL-1b、IL-6 和 IL-8 减少,Chit 和 TNF-α 与卒中严重程度相关。
观察到卒中后强烈的微环境激活,以及 SH 水平与免疫反应标志物之间的相关性表明,特别是在卒中患者中,维持氧化还原功能以防止脑损伤是必要的。SH 水平降低代表试图中和异常的自由基生成。由于缺血事件后大脑的再灌注代表了严重的氧化应激,必须通过氧化还原敏感功能的再生来纠正,因此在这种情况下,药物干预可能是有益的。