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The serum levels of IL-10 in the angioplasty-only group (group 1) were significantly different on day 3 after angioplasty compared with those 1 day before angioplasty (P [http://www.selleckchem.com/small-molecule-compound-libraries.html Small molecule library high throughput] triggers inflammatory reactions leading to the development of intimal hyperplasia. Atrial specimens from human restenotic lesions revealed an increased number of inflammatory cells and monocyte chemoattractant protein-1 in restenotic lesions (Moreno et al. 1996; Farb et al. 2002; Hokimoto et al. 2002). Farb et al. (2002) noted that coronary stenting induces increased arterial inflammation that is associated with increased neointimal [http://www.selleckchem.com/products/CAL-101.html selleck chemical] growth. Similar findings also indicated that stent implantation is associated with an increase in an acute-phase protein, C-reactive protein, which shows significantly higher serum levels for longer in patients with restenosis compared with those without restenosis (Gottsauner-Wolf et al. 2000; Almagor et al. 2003). A number of anti-inflammatory agents have been used in clinical trials to evaluate their efficiency in preventing neointimal hyperplasia. The REGRESS study (Regression Growth Evaluation Statin Study) suggested that pravastatin treatment reduced 2 year clinical and angiographic restenosis (Mulder et al. 2000). Use of non-specific anti-inflammatory agents, such as prednisone, for prevention of restenosis was investigated in the IMPRESS study (Immunosuppressive Therapy for the Prevention of Restenosis after Coronary Artery Stent Implantation), indicating that 6 month restenosis rate and lumen loss were lower in patients treated with prednisone (Versaci et al. 2002). Clinical trials of a drug-eluting stent [http://en.wikipedia.org/wiki/Ficain Ficain] coated with paclitaxel, an agent that has anti-inflammatory and antiproliferative properties, have demonstrated a reduction in coronary restenosis (Park et al. 2003; Stone et al. 2004). Interestingly, it has been reported that activated inflammatory cells increased the local temperature of the atherosclerotic plaque (Casscells et al. 1996), which is an independent predictor of clinical outcome in patients undergoing a percutaneous coronary intervention, showing the effect of pre-existing inflammation in the development of restenosis (Stefanadis et al. 2001).