PDF(Pubmed)
Abstract：
Two important factors affecting the progress of coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are the S-protein binding function of ACE2 receptors and the membrane fluidity of host cells. This study aimed to evaluate the effect of static magnetic field (SMF) on S-protein/ACE2 binding and cellular membrane fluidity of lung cells, and was performed in vitro using a Calu-3 cell model and in vivo using an animal model. The ability of ACE2 receptors to bind to SARS-CoV-2 spike protein on host cell surfaces under SMF stimulation was evaluated using fluorescence images. Host lung cell membrane fluidity was tested using fluorescence polarization to determine the effects of SMF. Our results indicate that 0.4 T SMF can affect binding between S-protein and ACE2 receptors and increase Calu-3 cell membrane fluidity, and that SMF exposure attenuates LPS-induced alveolar wall thickening in mice. These results may be of value for developing future non-contact, non-invasive, and low side-effect treatments to reduce disease severity in COVID-19-invaded lungs.
摘要：
影响由严重急性呼吸综合征冠状病毒2（SARS-CoV-2）引起的冠状病毒病2019（COVID-19）进展的两个重要因素是ACE2受体的S蛋白结合功能和宿主细胞膜流动性。本研究旨在评估静磁场（SMF）对肺细胞S蛋白/ACE2结合和细胞膜流动性的影响。并且使用Calu-3细胞模型在体外和使用动物模型在体内进行。使用荧光图像评估了ACE2受体在SMF刺激下与宿主细胞表面上的SARS-CoV-2刺突蛋白结合的能力。使用荧光偏振测试宿主肺细胞膜流动性以确定SMF的作用。我们的结果表明，0.4TSMF可以影响S蛋白与ACE2受体之间的结合并增加Calu-3细胞膜的流动性，SMF暴露减轻了LPS诱导的小鼠肺泡壁增厚。这些结果可能对发展未来的非接触式，非侵入性，和低副作用治疗，以降低COVID-19侵袭肺部的疾病严重程度。
