Discipline of Nutrition and Metabolism, Department of Pediatrics, Federal University of São Paulo, São Paulo, Brazil.
Discipline of Nutrition and Metabolism, Department of Pediatrics, Federal University of São Paulo, São Paulo, Brazil.
Transl Res. 2019 Jun;208:85-104. doi: 10.1016/j.trsl.2019.01.004. Epub 2019 Jan 19.
The role of the vascular endothelium in inflammation was demonstrated experimentally through biomarkers of endothelial dysfunction and cytoprotection. Selenium is a trace element essential for cell protection against oxidative lesions triggered by reactive oxygen species or inflammatory responses. Preclinical studies have demonstrated a relationship between adhesion molecules as biomarkers of endothelial dysfunction and selenoproteins as biomarkers of selenium status under conditions that mimic different diseases. Most studies in humans indicate an association between selenium deficiency and increased risk of morbidity and mortality, yet the pathophysiology of selenium in endothelial activation remains unknown. Here, we summarize selenium-dependent endothelial function evaluation techniques and focus on the role of selenium in endothelial cytoprotection according to current scientific knowledge. Most studies on the role of selenium in endothelial processes show selenium-dependent endothelial functions and explain how cells and tissues adapt to inflammatory insults. Taken together, these studies show an increase in adhesion molecules and a decrease in the expression of selenoproteins following a decreased exposure to selenium. Few clinical trials have enough methodological quality to be included in meta-analysis on the benefits of selenium supplementation. Furthermore, the methodology adopted in many studies does not consider the relevant findings on the pathophysiology of endothelial dysfunction. Preclinical studies should be more frequently integrated into clinical studies to provide clearer views on the role of selenium status in endothelial cytoprotection.
血管内皮在炎症中的作用通过内皮功能障碍和细胞保护的生物标志物得到了实验证明。硒是一种必需的微量元素，可保护细胞免受由活性氧或炎症反应引发的氧化损伤。临床前研究表明，在模拟不同疾病的条件下，黏附分子作为内皮功能障碍的生物标志物与硒蛋白作为硒状态的生物标志物之间存在关联。大多数针对人类的研究表明，硒缺乏与发病率和死亡率增加之间存在关联，但内皮激活中硒的病理生理学仍然未知。在这里，我们总结了依赖于硒的内皮功能评估技术，并根据当前的科学知识重点介绍了硒在内皮细胞保护中的作用。大多数关于硒在血管内皮细胞过程中的作用的研究表明，硒依赖的内皮功能，解释了细胞和组织如何适应炎症损伤。综上所述，这些研究表明，随着暴露于硒的减少，黏附分子增加，而硒蛋白的表达减少。很少有临床试验具有足够的方法学质量，无法纳入关于硒补充益处的荟萃分析。此外，许多研究采用的方法学并没有考虑到内皮功能障碍病理生理学的相关发现。应更频繁地将临床前研究纳入临床研究，以便更清楚地了解硒状态在内皮细胞保护中的作用。
