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

doi:10.16352/j.issn.1001-6325.2026.11.1477

Abstract

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

CLC Number:

CHANG Fengjun, WANG Ai, CHENG Gong, LI Hongwen. Aspirin inhibits vascular damage caused by circulating microparticles from stable angina patients[J]. Basic & Clinical Medicine, 2026, 46(11): 1477-1482.

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