将血小板用作神经元 "外周模型 "的药理学验证前景

Alexander L. Urakov, I. L. Nikitina, E. E. Klen, Yi Wang, A. Samorodov
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引用次数: 0

摘要

简介患有心血管系统疾病的患者中经常会出现抑郁症,而且抑郁症是心肌梗塞、急性缺血性脑血管意外、肺栓塞等血栓事件发生的预兆。有理由相信,这是由于血小板与脑神经元的结构和生化关系,使我们可以将血小板视为中枢神经系统病变的标志物。 本综述旨在从血小板作为神经元外周模型的角度,评估止血系统与抑郁症发病之间的关系,并评价治疗抑郁症药物的有效性。 材料和方法。研究工作按照《系统综述和元分析首选报告项目》(PRISMA)的建议进行。为进行本综述,使用 PubMed、Cochrane 和 CINAHL 数据库,按照关键词 "止血、急性脑血管意外、抑郁症、抑郁障碍、血小板、心血管疾病",对 2018 年至 2023 年期间的文献进行了系统检索。 研究结果所获得的数据表明,抑郁障碍与血管事件之间存在临床联系,血小板与中枢神经系统细胞之间存在共性,这是因为以下蛋白具有共性:5-羟色胺或5-羟色胺(5-HT)的转运体和受体、淀粉样前体蛋白(APP)和脑神经营养因子(BDNF),而这些蛋白之前被认为是特定的神经蛋白。此外,止血动态与抑郁症的药物治疗之间也有关系。 结论。在这篇综述中,我们认真分析了患有血管疾病的抑郁症患者在血小板活化方面的止血变化。文献中介绍的血小板诱导机制多种多样,需要进一步研究。通过对抑郁症患者血小板活化途径的合理研究,可以全面了解抑郁症患者止血与各种血管病变关系的分子机制本质。抑郁症患者的血小板活化以及抑郁障碍治疗过程中止血系统参数的动态变化,使我们能够将止血视为中枢神经系统和药物治疗的外周标志物。
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Prospects for pharmacological validation of the use of platelets as a "peripheral model" of neurons
Introduction. Depressive disorders are often found in patients with pathology of the cardiovascular system and are a predictor of the development of thrombotic events, such as myocardial infarction, acute ischemic cerebrovascular accident, pulmonary embolism. There are reasons to believe that this is due to the structural and biochemical relationship of platelets and brain neurons, which allows us to consider platelets as a marker of the pathology of the central nervous system. The purpose of this review is to assess the relationship between the hemostasis system and the development of depressive disorders from the standpoint of using platelets as a peripheral model of neurons and evaluating the effectiveness of drugs for the treatment of depression. Materials and methods. The work was carried out in accordance with the recommendations of Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA). For this review, a systematic literature search was conducted using PubMed, Cochrane and CINAHL databases for the period from 2018 to 2023, according to the keywords, hemostasis, acute cerebrovascular accident, depression, depressive disorders, platelets, cardiovascular diseases". Results. The data obtained indicate both a clinical link between depressive disorders and vascular events, and the commonality of platelets and CNS cells due to the commonality of the following proteins: transporters and receptors of serotonin or 5-hydroxytryptamine (5-HT), amyloid precursor protein (APP) and brain neurotrophic factor (BDNF), which previously they were considered specific neural proteins. In addition, there is a relationship between the dynamics of hemostasis and drug therapy for depression. Conclusions. In this review, we critically analyzed changes in hemostasis in terms of platelet activation in depressed patients with vascular disease. The mechanisms of platelet induction presented in the literature are diverse and require further study. A rational study of the pathways of platelet activation in patients with depressive disorders will provide a comprehensive understanding of the essence of the molecular mechanisms underlying the relationship of hemostasis in patients with depression in various vascular pathologies. Platelet activation in patients with depression and the dynamics of changes in hemostasis system parameters during the treatment of depressive disorders allows us to consider hemostasis as a peripheral marker of the central nervous system and pharmacotherapy.
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