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血管性血友病因子多聚体与松弛反应:一项为期一年的研究。

Von Willebrand Factor Multimers and the Relaxation Response: A One-Year Study.

作者信息

Dal Lin Carlo, Acquasaliente Laura, Iliceto Sabino, De Filippis Vincenzo, Vitiello Giuseppe, Tona Francesco

机构信息

Department of Cardiac, Thoracic and Vascular Sciences, Padua University School of Medicine, Via Giustiniani 5, 35131 Padua, Italy.

Department of Pharmaceutical and Pharmacological Sciences, Padua University School of Medicine, Via Marzolo 2, 35100 Padua, Italy.

出版信息

Entropy (Basel). 2021 Apr 10;23(4):447. doi: 10.3390/e23040447.

DOI:10.3390/e23040447
PMID:33920144
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8069424/
Abstract

BACKGROUND AND AIM

Mental stress represents a pivotal factor in cardiovascular diseases. The mechanism by which stress produces its deleterious ischemic effects is still under study but some of the most explored pathways are inflammation, endothelial function and balancing of the thrombotic state. In this scenario, von Willebrand factor (vWF) is a plasma glycoprotein best known for its crucial hemostatic role, also acting as key regulatory element of inflammation, being released by the activated vascular endothelium. Antistress techniques seem to be able to slow down inflammation. As we have recently verified how the practice of the Relaxation Response (RR), which counteracts psychological stress, causes favorable changes in some inflammatory genes' expressions, neurotransmitters, hormones, cytokines and inflammatory circulating microRNAs with coronary endothelial function improvement, we aimed to verify a possible change even in serum levels of vWF. Experimental procedure: We measured vWF multimers and the total protein carbonyl contents in the sera of 90 patients with ischemic heart disease (and 30 healthy controls) immediately before and after an RR session, three times (baseline, 6 months, 12 months), during a one-year follow-up study.

RESULTS

According to our data, large vWF multimers decrease during the RR, as does the plasma total carbonyl content.

CONCLUSION

vWF levels seem to vary rapidly between anti-inflammatory and antithrombotic behaviors dependent on psychological activity, leading to relaxation and also possibly changes in its quaternary structure.

摘要

背景与目的

精神压力是心血管疾病的一个关键因素。压力产生有害缺血效应的机制仍在研究中,但一些研究最多的途径是炎症、内皮功能和血栓状态的平衡。在这种情况下,血管性血友病因子(vWF)是一种血浆糖蛋白,因其关键的止血作用而最为人所知,它也是炎症的关键调节因子,由活化的血管内皮释放。抗压力技术似乎能够减缓炎症。由于我们最近证实了对抗心理压力的放松反应(RR)的实践如何导致一些炎症基因表达、神经递质、激素、细胞因子和炎症循环微小RNA发生有利变化,并改善冠状动脉内皮功能,我们旨在验证vWF血清水平是否也可能发生变化。实验步骤:在一项为期一年的随访研究中,我们在RR疗程前后立即测量了90例缺血性心脏病患者(以及30例健康对照)血清中的vWF多聚体和总蛋白羰基含量,共测量三次(基线、6个月、12个月)。

结果

根据我们的数据,RR期间大vWF多聚体减少,血浆总羰基含量也减少。

结论

vWF水平似乎会根据心理活动在抗炎和抗血栓行为之间迅速变化,从而导致放松,其四级结构也可能发生变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/919ea949fc01/entropy-23-00447-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/c23129c01137/entropy-23-00447-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/54f9e4e67f0f/entropy-23-00447-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/367da37a844e/entropy-23-00447-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/a060d8211e59/entropy-23-00447-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/919ea949fc01/entropy-23-00447-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/c23129c01137/entropy-23-00447-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/54f9e4e67f0f/entropy-23-00447-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/367da37a844e/entropy-23-00447-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/a060d8211e59/entropy-23-00447-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b12/8069424/919ea949fc01/entropy-23-00447-g005.jpg

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