锌(Ⅱ)诱导抗血栓形成对抗COVID-19严重感染

Dr. Sci. Tsuneo Ishida
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摘要

锌(Ⅱ)诱导的神经性COVID-19抗血栓形成已被证实,锌诱导的抑制性支气管血栓形成和调节性肺血栓栓塞,引起COVID-19激活的抗血栓活性,导致COVID-19抗血栓形成。锌补充影响支气管粘膜上皮的完整性,在正常和缺锌条件下,存在个体锌状态之间的相互作用。另一方面,锌离子抑制COVID-19肺部炎症,促进血小板活化功能,抑制肺血栓栓塞,其中血小板可响应细胞外和细胞内Zn2+浓度的变化。锌诱导血小板聚集、低浓度ZnSO4和锌螯合涉及血小板活化和血小板聚集增强,其中Zn2+在凝血调节中起主要作用,锌抑制血液凝固对抗COVID-19感染。Zn2+可以调节血小板和凝血激活途径,包括纤维蛋白的形成,离子Zn2+储存的释放有助于Zn2+在血小板依赖性纤维蛋白形成中的促凝作用。此外,锌可能会减少COVID-19患者的神经系统疾病,因为Zn2+可以促进炎症细胞因子作为神经退行性疾病,冠状病毒可以通过血液循环影响神经系统,引起神经炎症。锌离子可以抑制炎症、血小板行为功能和血液凝固。因此,锌离子促进ROS生成过程中的神经抗血栓形成和过度氧化应激,以对抗COVID-19感染。对于COVID-19严重恶化的成年人,建议持续锌摄入量为8-11毫克/天(最高摄入量为40毫克/天),并建议锌摄入量为30-70毫克/天可能有助于RNA病毒控制。因此,明确了Zn2+离子结合的分子机制,Zn2+离子可能通过以Zn2+离子为中心的四边形结合蛋白分子配位模式与COVID-19炎症、血小板、凝血、血栓等多种蛋白结合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Zinc (Ⅱ)-Induced Anti-Thrombus Formation against Severe COVID-19 Infection
Zinc(Ⅱ) induced neurological COVID-19 anti-thrombus formation has been established by that zinc induced inhibitive bronchial thrombosis and modulatory pulmonary thromboembolism are attained, causing COVID-19 activated anti-thrombus activity and leading to COVID-19 anti-thrombus formation. Zinc supplementation affected bronchial mucosal epithelial integrity, both under normal and zinc deficient conditions that there was an interaction between the individual zinc status. The other, zinc ions inhibit COVID-19 lung inflammation and promote platelet activation function that inhibits pulmonary thromboembolism, in which platelets could respond to changes in extracellular and intracellular Zn2+ concentration. Zinc-induced platelet aggregation, low concentrations of ZnSO4 and zinc chelation involve platelet activation and potentiated platelet aggregation, in which Zn2+ plays a major role in the regulation of coagulation that zinc inhibit blood coagulation against COVID-19 infection. Zn2+ can modulate platelet and coagulation activation pathways, including fibrin formation that the release of ionic Zn2+ store contributes to the procoagulant role of Zn2+ in platelet-dependent fibrin formation. Further, zinc may reduce neurological resultings in COVID-19 patients that Zn2+ promotes inflammatory cytokine as a neurodegenerative disorder and the coronaviruses can affect the nervous system through blood circulation, causing neuro-inflammation. Zinc ions can inhibit inflammation, platelet behaviour function, and blood coagulation. Hence, zinc ions promote neurological anti-thrombosis formation during ROS production and excessive oxidative stress against COVID-19 infection. Persistent zinc intake for severe aggravation of COVID-19 has been suggested to be 8–11 mg/day for adults (upper intake level 40 mg/day) and suggesting that a zinc intake of 30–70 mg/day might aid in the RNA virus control. Accordingly, Zn2+ ions-binding molecular mechanism has been clarified that Zn2+ ions may be bound with COVID-19 inflammatory, platelet, coagulation, and thrombus various proteins by Zn2+ ions-centered tetrahedrally binding protein molecular coordination pattern.
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