摘要
目的观察氟伐他汀动员急性心肌梗死(AMI)大鼠内皮祖细胞(EPCs),促进梗死心肌血管新生,减小梗死面积的效果。方法①成年Wistar大鼠左前降支结扎造模,随机分为空白组(A组)、假手术组(B组)、AMI组(C组)和氟伐他汀治疗AMI组(D组)。②流式细胞技术检测不同时段大鼠外周静脉血EPC动态变化。③4周末处死大鼠,心肌切片Masson染色,左室心肌正中线弧长方法计算梗死面积。④CD31单克隆抗体免疫组化法标记心肌新生血管内皮细胞并计算各组梗死、梗死周边及非梗死区新生血管数。结果①造模后第7天D组EPCs(37.13±3.44/2×10^5MNCs)显著高于A组(19.88±4.91/2×10^5MNCs)、B组(22.33±5.43/2×10^5MNCs)和C组(26.56±3.17/2×10^5MNCs),差异具有统计学意义(P〈0.05);C组较A组有少量增加(P〈0.05),B组较A组无明显升高(P〉0.05),B组和c组差异无统计学意义(P〉0.05)。造模后第14天D组EPCs(45.5-±4.99/2×10^5MNCs)同样显著高于A组(17.25±7.17/2×10^5MNCs)、B组(22.78±2.91/2×10^5MNCs)和C组(26.88±3.76/2×10^5MNCs)(P〈0.05);B组和C组较A组有少量增加(P〈0.05),B组和C组差异无统计学意义(P〉0.05)。第7天和第14天各组变化比较,A、B、C三组EPCs变化无统计学意义(P〉0.05),D组则明显增加(P〈0.05)。②D组梗死区新生血管计数(10.75±1.61/mm。)明显多于C组(5.09±2.33/mm。)(P〈0.01),梗死周边区新生血管计数D组(17.53±2.35/mm^2)同样明显多于C组(8.55±2.40/mm^2)(P〈0.01)。③D组梗死面积[(31.41±2.59)%]小于C组[(35.67±5.22)%](P〈0.01)。结论①氟伐他汀能动员急性心肌梗死大鼠内皮祖细胞进入外周血循环,使其数量增加并促进梗死周边区血管新生。②心肌梗死后大鼠应用氟伐他汀可以限制梗死面积。
Objective To observe the effect of fluvastatin on endothelial progenitor cells (EPCs) mobi- lization in Wistar rats with acute myocardial infarction (AMI), and the consequences of myocardial neovasculariza-tion and myocardial infarction size restriction. Methods (1) Adult Wistar rats were randomly divided into 4 groups: normal control group (A), sham operation group(B), AMI group(C), AMI treated with Fluvastatin (D). (2)Peripheral venous blood were drew at day 7 and 14 after AMI to detect the EPCs by flow cytometry analysis. (3) The infarct size was calculated by the method of measuring left ventricular midline infarct arc length. (4)Immunohis-tochemical stain of anti-rat CD31 monoclonal antibody was used to detect the density of myocardial neovasculariza-tion in myocardial infarction region, periinfarction region and non infarction region. Results (1)At 7th days after AMI, the number of EPCs in group D (37.13±3.44/2×10^5 MNCs) increased significantly than those in group A (19.88±4.91/2×10^5 MNCs), group B (22.33±5.43/2×10^5 MNCs) and group C (26.56±3.17/2×10^5 MNCs)(P〈 0.05), and the number of EPCs in group C increased slightly than those in group A (P〈0.05), the number of EPCs in group B didn't increased than those in group A (P〉0.05), there were no significant statistical difference among group B and C (P〉O.05). And 14th days after AMI, the number of EPCs in group D (45.5±4.99/2×10^5 MNCs) increased also significantly than those in group A(17.25±7.17/2×10^5 MNCs), group B(22.78±2.91/2×10^5 MNCs) and group C (26.88±3.76/2±105 MNCs)(P〈0.05), and the number of EPCs in group C and group B in-creased slightly than those in group A(P〈0.05 ), there were no significant statistical difference among group B and C (P〉0.05). Between the numbers of EPCs at day 7 and day 14, there were no significant statistical diference in group A, B and C (P〉0.05), but there were significant increasing in group D(P〈0.05). (2)The capillary densitiy in myocardial infarction were higher in group D (10.75±1.61/mm^2) than in group C(5.09±2.33/mm^2) (P〈0.01), and in periinfaction region, the capillary densitiy were also higher in group D (17.53±2.35/mm^2) than in group C (8.55±2.40/mm^2) (P〈0.01). (3) The infarct size in group D (31.41±2.59)% was smaller than that in group C (35.67±5.22)%(P〈0.01). Conclusion (1)Fluvastatin could mobilize EPCs into peripheral circulation and pro-mote myocardial neovaseularization in rats with AMI. (2)Fluvastatin could restrict infarct size.
出处
《中国心血管病研究》
CAS
2012年第11期859-864,880,共7页
Chinese Journal of Cardiovascular Research
基金
天津市卫生局科技基金项目(项目编号:06KY19)
关键词
祖细胞
心肌梗塞
新生血管
Progenitor cells
Myocardial infarction
Neovascularization