Interleukin-10 inhibits intimal hyperplasia after angioplasty or stent implantation in hypercholesterolemic rabbits

Article

关键词: ATHEROSCLEROTIC LESIONS;    CYTOKINE PRODUCTION;    HUMAN MONOCYTES;    BALLOON INJURY;    IL-10;    MACROPHAGES;    RESTENOSIS;    ARTERY;    RECRUITMENT;    MECHANISMS;   

DOI  :  10.1161/01.CIR.101.8.908

来源: SCIE

【 摘 要 】

Background-Intimal hyperplasia after stent implantation is the main cause of in-stent restenosis. Activated monocytes play a key role in intimal growth. The anti-inflammatory cytokine interleukin-10 (IL-10) is a potent monocyte deactivator, endogenously produced in the atherosclerotic plaque. We tested the hypothesis that exogenous IL-10 may limit postangioplasty intimal hyperplasia after balloon angioplasty or stenting, Methods and Results-Hypercholesterolemic rabbits were treated with recombinant human IL-10 (rhuIL-10) for 3 days after balloon angioplasty or 28 days after stent implantation, High IL-10 serum levels and intense deactivation of circulating monocytic cells, assessed by inhibition of IL-1 beta release by lipopolysaccharide-stimulated whole blood, were detected for at least 8 hours after rhuIL-10 intravenous injection (ELISA). Morphometric analyses, performed 28 days after injury, indicated that rhuIL-10 reduced intimal growth by approximate to 50% after balloon angioplasty or stenting, resulting in more preserved lumen in stented arteries. Moreover rhuIL-10 reduced macrophage infiltration by 67% and proliferative activity by 81% in the intima and the: media. No toxic effect was detected except minor changes in blood cell count, Conclusions-The anti-inflammatory cytokine rhuIL-10 reduces postinjury intimal hyperplasia. The potent attenuation of in-stent intimal growth by rhuIL-10 and its favorable toxicity profile prevention of in-stent restenosis.

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