Abstract

Lectin-like oxidised low-density lipoprotein receptor-1 (LOX-1) is a membrane protein that can support the binding, internalisation, and proteolytic degradation of oxidised low-density lipoprotein. The LOX-1 expression and superoxide generation increases in the neointima after balloon injury. Cilostazol, a well-know phosphodiesterase type 3(PDE3) inhibitor for the treatment of peripheral arterial disease, has vasodilator properties and an anti-proliferative action on the growth of vascular smooth muscle cells. To investigate whether cilostazol suppresses intimal hyperplasia and to elucidate its mechanism, we examined the effects of cilostazol to the expression of LOX-1 mRNA and protein, superoxide generation and neointimal hyperplasia of the rat carotid artery after balloon injury. The injury was performed inserting the balloon catheter through the rat common carotid artery and after 14 days a histopathological analysis revealed a significant restenosis with smooth muscle cell proliferation and neointima formation that was associated with an enhanced expression of LOX-1, superoxide generation, Pretreatment of rats with cilostazol (100 mg/kg/day) reduced neointima formation, superoxide generation, and LOX-1 expression (p<0.05). Here, we show that Cilostazol reduces neointimal hyperplasia by inhibition superoxode generation and expression of lectin-like oxidised LDL receptor-1 after balloon common arterial injury in a rat model.