Stent-based delivery of triptolide reduces neointimal formation in rabbit iliac arteries

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The long-term clinical efficacy of intracoronary stenting is limited by restenosis, which occurs in 15% to 30% of patients.1 In-stent restenosis is solely due to neointimal hyperplasia. Stent-based delivery of sirolimus, which inhibits intimal proliferation by blocking the G1/S transition, has been successfully used to prevent in-stent restenosis in clinical practice. Previous studies have shown that triptolide inhibited the DNA synthesis of vascular smooth muscle cells by blocking the transition from G0/G1 to S phase,2 suggesting that triptolide could be useful for preventing restenosis. The potential unwanted side effects limits the use of systemic administration of this agent for the prevention of in-stent restenosis. Local delivery using a stent platform, however, might allow deposition of a therapeutic triptolide concentration in the arterial wall, with a substantially reduced risk of systemic toxicity. The purpose of the present study was to determine the efficacy of stent-based delivery of triptolide.
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