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作 者:王改玲[1] 肖传实[1] 邱龄[1] 赵文燕[1]
机构地区:[1]山西医科大学第二临床医学院心内科,030001
出 处:《国际心血管病杂志》2006年第1期56-59,共4页International Journal of Cardiovascular Disease
基 金:吴阶平医学基金(2003-97-A)
摘 要:目的:探讨不同剂量的阿托伐他汀在不同时相对内皮前体细胞(EPC)的动员作用。方法:将雄性新西兰兔随机分为4组:正常对照组、阿托伐他汀2.5mg、5mg、10mg组。用药后1、2、3、4周分别测量外周血EPC含量。用流式细胞仪计数EPCs,PE-CD34/FITC-CD133双阳性细胞为EPC;荧光显微镜鉴定FITC-UEA-1/Dil-acLDL双染色阳性细胞为EPC。用药第3周测血清一氧化氮(NO)、血脂。结果:用药后1、2、3、4周四组外周血EPCs的曲线:正常对照组为一低水平基线;阿托伐他汀5mg组、阿托伐他汀2.5mg组(按作用从大到小排列)为锯齿样曲线,第二周最低,第三周最高,第四周较第三周低;阿托伐他汀10mg组与正常组接近,仅第四周增高(P<0.05)。阿托伐他汀5mg组对EPCs有持续动员作用,于第三周时效果最佳,约为第一周的3倍,是正常组的近20倍;阿托伐他汀2.5mg组在第三、四周有作用。在第四周,三个用药组EPCs均较正常组高,且用药三组间无统计学差异。与正常组相比,阿托伐他汀5mg组血清NO增高,阿托伐他汀10mg组NO降低。各组血脂均在正常范围内。结论:不同剂量阿托伐他汀对EPCs均有动员作用,其效果为:5mg组>2.5mg组>10mg组。阿托伐他汀5mg组在第三周效果最佳。阿托伐他汀对EPCs的动员可能与NO有关。Objective:To evaluate the effects of atorvastatin at various dose regimes on the mobilization of endothelial progenitor cells (EPCs). Methods: 32 male New Zealand rabbits were equally divided into 4 groups: normal control, atorvastatin 2.5 mg, atorvastatin 5 mg and atorvastatin 10 mg group. The number of EPCs was determined both as PE-CD34 /FITC CD133 dual-stained positive cells by flow cytometry analysis and as cells double positive for FITC-UEA-1 and Dil-acLDL by fluorescent microscope at 1, 2, 3 and 4 weeks after administration. At the third week, serum nitric oxide (NO) and serum lipid levels were also measured. Results:Comparing with normal control group, the number of EPCs in atorvastatin 5 mg group was significantly increased at the first week and led to 20-fold increase at the peak of the third week (P〈0.01) ; 2.5 mg atorvastatin significantly increased EPCs numbers at third week (P〈0.05), but 10mg atorvastatin only at the forth week (P〈0.05). Serum NO levels in atorvastatin 5mg group were higher and in atorvastatin 10 mg group were lower in comparison with normal control group. Whereas no difference was observed in serum lipid levels among the 4 groups. Conclusion: 5 mg atorvastatin is the best dose for mobilizing EPCs. The mechanism of mobilization for statin treatment might be relate to increasing NO independent of its modulation to serum lipids.
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