氧化还原状态在covid -19相关性肺炎重症患者血小板功能障碍中的作用

Mikhail V. Osikov, V. Antonov, S. Zotov, G. Ignatova
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摘要

背景:COVID-19患者血小板功能障碍是一个众所周知的事实;然而,其形成机制尚不清楚。目的:探讨氧化应激在重症covid -19相关性肺炎患者血小板功能障碍中的作用。材料和方法:该研究纳入了47 - 75岁的COVID-19患者(n = 27),胸部多层计算机断层扫描显示肺损伤超过50%。对照组包括性别和年龄相仿的健康人(n = 24)。所有患者均行血小板计数测定,二磷酸腺苷、胶原蛋白、肾上腺素、里斯托西汀诱导血小板聚集测定,富血小板血浆中脂质过氧化和蛋白氧化修饰产物水平测定。使用IBM SPSS Statistics v. 23对获得的数据进行了计算和分析。结果:重症COVID-19患者血液中血小板数量减少具有特征性。第1天观察到胶原蛋白和里斯托司汀诱导血小板聚集加速,入院第8天观察到二磷酸腺苷、胶原蛋白、肾上腺素和里斯托司汀诱导血小板聚集加速。COVID-19中的氧化应激导致血小板中蛋白质氧化修饰的主要标记物水平显著升高,血小板中初级和次级脂质过氧化标记物的产物水平升高。血小板中脂质过氧化产物和蛋白质氧化修饰及其聚集之间存在直接关联。结论:以下研究加深了对SARS-CoV-2感染过程中氧化应激状态的认识,证实了其在COVID-19发病机制中的重要作用。重症covid -19相关性肺炎患者在病程中蛋白氧化修饰和脂质过氧化产物的生长可能是血小板功能障碍的原因之一,从而导致致命性血栓并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of redox status in platelet dysfunction in severe COVID-19-associated pneumonia
BACKGROUND: Platelet dysfunction in patients with COVID-19 is a well-known fact; however, its formation mechanisms remain unclear. AIM: To evaluate the role of oxidative stress in dysfunction of platelets in the patients with severe COVID-19-associated pneumonia. MATERIALS AND METHODS: The study has involved patients with COVID-19 (n = 27) aged 47 to 75 with more than 50% lung damage according to the chest multi-slice computed tomography. The control group has included healthy people comparable in sex and age (n = 24). All the patients have undergone evaluation of the number of platelets in blood, measurement of platelet aggregation induced by adenosine diphosphate, collagen, adrenaline and ristocetin and the level of lipid peroxidation and protein oxidative modifications products in platelet-rich plasma. The calculation and analysis of the obtained data has been carried out using the IBM SPSS Statistics v. 23. RESULTS: For the patients with severe COVID-19, a decrease in the number of platelets in the blood is characteristic. Acceleration of platelet aggregation induced by collagen and ristocetin has been observed on the 1st day, with the induction of adenosine diphosphate, collagen, adrenaline and ristocetin on the 8th day of the admission. Oxidative stress in COVID-19 leads to a significant increase in the level of primary markers of protein oxidative modifications in the platelets and an increase in the level of products of primary and secondary lipid peroxidation markers in the platelets. A direct correlation between the products of lipid peroxidation and protein oxidative modifications in the platelets and their aggregation has been found. CONCLUSIONS: The following study deepens the knowledge of the status of oxidative stress in SARS-CoV-2 infection, confirming its important role in the pathogenesis of COVID-19. The growth of protein oxidative modifications and lipid peroxidation products in patients with severe COVID-19-associated pneumonia in the course of the disease may be one of the causes of platelet dysfunction and, as a result, lead to lethal thrombotic complications.
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