| 초록 |
Restenosis is currently the major limitation of percutaneous transluminal coronary angioplasty (PTCA), as seen in up to 30 to 40% of patients. Vascular smooth muscle cell (VSMC) migration and proliferation occur as early as 36h after aterial injury. These events cause neointimal thickening of vessel wall, which results in coronary artery diseases. Recent studies have reported a protective effect of 17β-estradiol(E2) on VSMC proliferation and migration. In this study, E2 is immobilized on surface of stent and its release from stent was studied in vitro. Stainless steel was activated by silane deposition and acrylic acid was grafted by glow discharge plasma polymerization. E2 was immobilized by esterification using Dicyclohexyl carbodiimide (DCC). Modified surfaces was characterized by Electron spectroscopy for Chemical Analysis (ESCA), Attenuated total reflectance-Fourier transform infrared (ATR-FTIR) spectroscopy and static water contact angle measurement, respectively. The amount of immobilized E2 was estimated by UV-visble spectrophotometer and HPLC. In-vitro release of E2 from stainless steel surface was also investigated by HPLC analysis. A novel method of estrogen immobilization onto metallic stent surface using plasma polymerization has been developed.
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