实用医学杂志 ›› 2022, Vol. 38 ›› Issue (4): 459-463.doi: 10.3969/j.issn.1006⁃5725.2022.04.012

• 临床研究 • 上一篇    下一篇

抗凝治疗与房颤患者血浆神经源性外泌体中T⁃tau 蛋白和Aβ1⁃42含量变化的关系

杜美玲 王晓元 张爱爱 郝翠君 张鹏祥   

  1. 河北北方学院附属第一医院（河北张家口 075400）

  • 出版日期:2022-02-25 发布日期:2022-02-25
  • 基金资助:
    河北省医学科学研究重点课题计划（编号：20170799）；张家口市科学技术研究与发展计划项目（编号：1711041H）

Relationship between anticoagulant therapy and concentration change of T⁃tau protein and Aβ1⁃42proteinin plasma neurogenic exosomes in patients with atrial fibrillation

DU Meiling，WANG Xiaoyuan，ZHANGAiai，HAO Cuijun，ZHANG Pengxiang.   

  1. The First Affiliated Hospital of Hebei North University，Zhangjiakou075400，China

  • Online:2022-02-25 Published:2022-02-25

摘要：

目的 研究抗凝治疗对永久性心房颤动患者血浆神经源性性外泌体中 T⁃tau 蛋白和 Aβ1⁃42含量的影响，评价抗凝治疗对房颤患者认知功能的影响。方法 共纳入140名年龄在50 ~ 75岁之间且既往无脑血管事件的永久性房颤患者，按照是否进行抗凝治疗分为抗凝治疗组及未进行抗凝治疗组。使用简易精神状态检查（MMSE）来评估所有患者的认知功能。采用 logistic 回归分析探讨抗凝治疗对房颤患者认知功能的影响；所有患者采集空腹静脉血，通过免疫沉淀法富集神经源性外泌体，并通过透射电镜和Western blot 鉴定外泌体存在，ELISA 法定量分析外泌体中 T⁃tau 蛋白及 Aβ1⁃42 的含量。分析两组患者神经源性外泌体中 T⁃tau 蛋白和 Aβ1⁃42 浓度的差异。结果 校正人口统计学特征和共病条件后，房颤患者未抗凝治疗与认知功能障碍显著相关（OR = 5.024，95%CI：1.584 ~ 15.936，P < 0.01）；未抗凝治疗组房颤患者认知功能障碍较抗凝治疗组显著增加（P < 0.001）；未抗凝治疗组外泌体中 T⁃tau 蛋白及 Aβ1⁃42 的浓度（221.75 ± 54.34 pg/mL 和3.97 ± 1.20 pg/mL）显著高于抗凝治疗组（183.02 ± 46.84 pg/mL和3.09 ± 0.79 pg/mL）（P < 0.001）。结论 抗凝治疗是永久性房颤患者认知功能的保护因素，可以延缓认知功能障碍相关蛋白的增长。

关键词:

永久性房颤, 神经源性外泌体, 认知功能障碍, 抗凝治疗, T?tau, Aβ1?42

Abstract:

Objective To study the relationship between anticoagulant therapy and concentration changesof T⁃tau protein and Aβ1⁃42 in plasma neurogenic exosomes in patients with permanent atrial fibrillation（AF），and then to evaluate the effect of anticoagulant therapy on cognitive function in AF patients. Methods A total of140 permanent AF patients aged 50 ~ 75 without previous cerebrovascular events were enrolled in this study. Theywere divided into two groups according to whether anticoagulant therapy was performed，40 patients in anticoagulantgroup and 100 patients in non⁃anticoagulant group. We used Mini Mental State Examination（MMSE）to assess thecognitive function of all participants. Logistic regression analysis was used to explore the effect of anticoagulanttherapy on cognitive function in patients with AF. We collected fasting venous blood from all subjects and enrichedneuronal⁃derived exosomes by immunoprecipitation，then confirmed exosomes by transmission electron microscopeand western blot. Quantitative analysis of T⁃tau protein and Aβ1⁃42 in exosomes was conducted by ELISA. Thedifference of protein concentration in neurogenic exosomes between the two groups was tested. Results Afteradjustment for demographic characteristics and comorbid conditions，non⁃anticoagulant therapy in patients with AFwas significantly associated with CI（OR = 5.024，95%CI：1.584 ~ 15.936，P < 0.01）. The cognitive impairment ofpatients with AF in non⁃anticoagulant group was significantly severer than that in anticoagulant group（P < 0.001）.The concentration of T⁃tau protein and Aβ1⁃42 in plasma neuronal⁃derived exosomes in non⁃anticoagulant group（221.75 ± 54.34 pg/mL and 3.97 ± 1.20 pg/mL）was significantly higher than that in anticoagulant group（183.02± 46.84 pg/mL and 3.09 ± 0.79 pg/mL）（P < 0.001）. Conclusion Anticoagulant therapy is a protective factor forcognitive function in patients with permanent AF and delays the growth of markers related to cognitive impairment.

Key words:

permanent atrial fibrillation, neuronal?derived exosomes, cognitive impairment, antico?agulant therapy, T?tau, Aβ1?42

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