基础医学与临床 ›› 2026, Vol. 46 ›› Issue (11): 1477-1482.doi: 10.16352/j.issn.1001-6325.2026.11.1477

• 研究论文 • 上一篇    下一篇

阿司匹林抑制稳定性心绞痛患者循环微粒对血管的损害

常凤军1, 王嫒2*, 程功3, 李红文1*   

  1. 1.陕西省人民医院 心血管内三科,陕西 西安 710068;
    2.蓝田县人民医院 心内科,陕西 西安 710500;
    3.西安市红会医院 心内科,陕西 西安 710054
  • 收稿日期:2025-09-24 修回日期:2026-01-27 出版日期:2026-11-05 发布日期:2026-10-26
  • 通讯作者: *18329586718@163.com;18792916588@163.com
  • 基金资助:
    陕西省自然科学基金(2020JM-666)

Aspirin inhibits vascular damage caused by circulating microparticles from stable angina patients

CHANG Fengjun1, WANG Ai2*, CHENG Gong3, LI Hongwen1*   

  1. 1. Third Department of Cardiology, Shaanxi Provincial People′s Hospital, Xi′an 710068;
    2. Department of Cardiology, Lantian County People′s Hospita, Xi′an 710500;
    3. Department of Cardiology, Honghui Hospital, Xi′an 710054, China
  • Received:2025-09-24 Revised:2026-01-27 Online:2026-11-05 Published:2026-10-26
  • Contact: *18329586718@163.com;18792916588@163.com

摘要: 目的 检测阿司匹林是否影响循环微粒(MPs)的功能。方法 检测健康受试者、服用阿司匹林前、后的稳定型心绞痛(SA)患者的MPs。然后以各组MPs孵育大鼠胸主动脉后,Western blot检测ERK1/2、p38 MAPK的表达;ELISA测定人血管内皮细胞黏附分子1(VCAM-1);化学法测定一氧化氮(NO)和超氧阴离子水平。结果 与健康受试者(3.01±0.72)mg/mL相比,SA患者的MPs浓度[(5.70±0.76)mg/mL]升高(P<0.05),阿司匹林组MPs浓度[(4.08±0.95)mg/mL]有所降低(P<0.05)。SA患者的MPs下调ERK1/2的表达(P<0.05),增加p38的表达、增加VCAM-1[control:(0.55±0.09)ng/mg protein; SA组:(1.17±0.13)ng/mg protein]和超氧阴离子[control:(0.53±0.07)RLU/sec/mg protein; SA组:(1.64±0.23)RLU/sec/mg protein]水平(P<0.05),降低NO含量[control:(2.23±0.67)μmol/g protein; SA组:(1.16±0.37)μmol/g protein](P<0.05)。阿司匹林一定程度上抑制MPs的上述功能。结论 阿司匹林通过对ERK/p38蛋白及氧化应激的调节部分阻断MPs的促炎、氧化应激、促凝和粘附特性,研究提示阿司匹林除抗血小板聚集外有保护心血管功能。

关键词: 循环微粒, 氧化应激, 抗栓, 稳定型心绞痛

Abstract: Objective To detect whether aspirin affects the function of circulating particles (MPs). Methods MPs of healthy subjects and stable angina (SA) patients before and after taking aspirin were examined. Then, the thoracic aorta of rats was incubated with MPs from each group to test the effects of MPs on ERK1/2 and p38 MAPK expression with Western blot, the level of adhesion molecule 1(VCAM-1) with ELISA, nitric oxide(NO) and superoxide radical with chemical method. Results Compared with healthy subjects[(3.01±0.72)mg/mL], MPs increased in SA patients[(5.70±0.76)mg/mL](P<0.05), but decreased after taking of aspirin[(4.08±0.95)mg/mL](P<0.05). MPs in SA patients reduced the expression of ERK1/2(P<0.05), increased the expression of p38 (P<0.05), increase VCAM-1[control:(0.55±0.09)ng/mg protein; SA:(1.17±0.13)ng/mg protein]and super oxide radical[control:(0.53±0.07)RLU/sec/mg protein; SA:(1.64±0.23)RLU/sec/mg protein] levels(P<0.05), and reduce NO generations compared to control:(2.23±0.67)μmol/g protein; SA:(1.16±0.37)μmol/g protein(P<0.05). Aspirin partly inhibits the functions of MPs. Conclusions Aspirin can partially block the pro-inflammatory, oxidative stress, procoagulant, and adhesive properties of MPs by regulating ERK/p38 protein and oxidative stress, which is believed to be a new protective mechanism in addition to antithrombotic effect.

Key words: circulating particle, oxidative stress, antithrombosis, stable angina pectoris

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