Endothelial damage effects of circulating microparticles from patients with stable angina are reduced by aspirin through ERK/p38 MAPKs pathways

IntroductionPlatelet activation participates in the development of both coronary artery disease (CAD) and circulating microparticles (MPs). As a commonly used medicine for coronary heart disease, whether aspirin affects the function of MPs remains unclear. AimsThis study was designed to test MPs from healthy subjects, and stable angina (SA) patients before and after aspirin administration were obtained. MPs origins were tested by flow cytometry. Rat thoracic aortas were incubated with MPs (with or without aspirin) to determine the effects of MPs on expression of ERK1/2, JNKs, and p38 MAPK. Affect on levels of NF-B, VCAM-1, NO, and O2-. ResultsCompared with healthy subjects, MPs concentrations increased in SA patients, but decreased after aspirin administration. According to flow cytometry, aspirin mainly decreased platelet-derived MP. MPs from SA patients decreased the expression of ERK1/2, increased expression of p38 MAPKs, JNKs. Increased NF-B, VCAM-1, and (O2-) levels decreased NO content. Aspirin therapy significantly inhibited function of MPs from SA patients, and pathway inhibitors (ERK1/2 inhibitor PD98059, p38 MAPKs inhibitor SB203580, NF-kB inhibitor PDTC) show similar effects with aspirin. ConclusionThese results indicate that the pro-inflammatory, oxidative stress, procoagulant, and adhesion properties of MPs can be partly blocked by aspirin via the ERK-NO/O2- and p38 -NF-B-VCAM-1 signal pathway, which clarified other functions beyond anti-atherothrombotic of aspirin.