Gong Cheng1, Xue-Feng Shan2, Xu-Lang Wang3, Wei-Wei Dong4, Zhe Li1, Xin-Hong Liu1, Wei Zhang1, Kun Xing1, Feng-Jun Chang1. 1. Department of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China. 2. Department of Children's Cardiac surgery, First Affiliated Hospital of Xinjiang Medical University, Urumuqi, Xinjiang, China. 3. Department of Nursing, Xian'yang Vocational and Technical College, Xian'yang, Shaanxi, China. 4. Xinjiang Petroleum Institute, Urumuqi, Xinjiang, China.
Abstract
INTRODUCTION: Platelet 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. AIMS: This 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-κB, VCAM-1, NO, and O2-. RESULTS: Compared 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-κB, 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. CONCLUSION: These 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-κB-VCAM-1 signal pathway, which clarified other functions beyond anti-atherothrombotic of aspirin.
INTRODUCTION: Platelet 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. AIMS: This 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-κB, VCAM-1, NO, and O2-. RESULTS: Compared 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-κB, 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. CONCLUSION: These 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-κB-VCAM-1 signal pathway, which clarified other functions beyond anti-atherothrombotic of aspirin.
Authors: Marta Brambilla; Maria Talmon; Paola Canzano; Luigia G Fresu; Sandra Brunelleschi; Elena Tremoli; Marina Camera Journal: Int J Mol Sci Date: 2022-04-27 Impact factor: 6.208