Tissue factor (TF) is a potent initiator of the coagulation cascade situated within the vessel wall as well as an important key sentinel in the pathogenesis of thrombosis and restenosis after balloon angioplasty. While TF is expressed not only on endothelial cell but also on innate immunocytes such as monocytes and macrophages, pathogenic environment culminates TF expression and release, leading to acute coronary syndrome or restenosis after balloon angioplasty. Recent basic studies focus on the therapeutic inhibition of tissue factor. Cilostazol, even though it is classically known as not TF inhibitor but AMP-PDE inhibitor, is clinically effective because of its possible antithrombic, vasodilating, antimitogenic, and cardiotonic action. However the underlying mechanism of cilostazol affected on restenosis is unclear. To clarify this issue, we primarily examined the effect of the cilostazol on TF expression by HUVECs and monocytes. HUVECs and CD14+ monocytes isolated from whole blood of healthy volunteers were incubated for 30minutes with or without cilostazol (1, 10, 100 關M). And then, HUVECs were treated with 10ng/ml TNF-慣and CD14 + monocytes with 1 關g/ml LPS, and incubated for 4 hours for RT-PCR or for 24 hours for western blotting. In HUVECs, expression of TF mRNA and TF by TNF-慣 was downregulated by cilostazol pretreatment in dose dependant manner. This downregulation was similar in CD14+ monocytes. In conclusion, these data indicate that cilostazol act as a TF inhibitor on HUVECs and monocytes, and that cilostazol is potent inhibitor of restenosis possibly resulted by percutaneus transluminal coronary angioplasty.