作者: C. Napoli , G. Cirino , P. Del Soldato , R. Sorrentino , V. Sica
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摘要: Restenosis is due to neointimal hyperplasia, which occurs in the coronary artery after percutaneous transluminal angioplasty (PTCA). During restenosis, an impairment of nitric oxide (NO)-dependent pathways may occur. Concomitant hypercholesterolemia exacerbate restenosis patients undergoing PTCA. Here, we show that a NO-releasing aspirin derivative (NCX-4016) reduces degree balloon low-density lipoprotein receptor-deficient mice and this effect associated with reduced vascular smooth muscle cell (VSMC) proliferation macrophage deposition at site injury. Drugs were administered following both therapeutic or preventive protocols. We demonstrate NCX-4016 effective prevention treatment presence hypercholesterolemia. These data indicate NO-dependent mechanisms be involved development hypercholesterolemic mice. Although experimental models not reflect humans all details, suggest could drug reducing PTCA, especially and/or gastrointestinal damage.