摘要
目的通过人体药物临床试验,观察不同剂量阿托伐他汀钙对冠心病患者外周血内皮祖细胞(EPC)增殖、迁移、黏附及血管修复能力的影响。方法选择冠心病患者40例,根据服用阿托伐他汀钙的剂量不同,分为小剂量组(20mg)20例及大剂量组(40mg)20例。所有入选患者于服药前服药5、15、30、60、90和120d分别抽取外周血获取外周血单个核细胞,体外培养后进行细胞染色与鉴定、MTT比色法检测细胞增殖、检测EPC的迁移及黏附能力,流式细胞仪分析EPC标记表面CD34、CD133、人血管内皮细胞生长因子受体2(VEGFR-2)的表达。结果EPC的迁移能力在30d时最强,30d后大剂量组迁移能力的下降趋势显著高于小剂量组(P<0.05,P<0.01);EPC增殖、黏附和CD34的表达在60d时达高峰;CD133在30d时最低,而此后大剂量组成熟EPC的下降率显著高于小剂量组;VEGFR-2的细胞表达在60d后呈持续下降趋势,而小剂量组VEGFR-2明显高于大剂量组(P<0.05,P<0.01)。结论长期使用阿托伐他汀钙并不能有效促进EPC的活化及新生血管的生成。20mg的阿托伐他汀钙对血管内膜的修复更优于40mg。
Objective To study the effect of different atorvastatin doses on proliferation,adhesion,migration,differentiation and vascular intima repair of endothelial progenitor cells(EPC)in CHD patients.Methods Forty CHD patients were divided into 20 mg atorvastatin group and 40 mg atorvastatin group(20in each group).Their peripheral mononuclear cells were calculated,cultured,and stanined.The proliferation,adhesion,migration of EPC were assayed by MTT colorimetry.Expressions of surface CD34,CD133,and VEGFR-2in EPC were detected by cytometry.Results The migration of EPC reached its peak on day 30,and decreased more significantly from day 30 in 40mg atorvastatin group than in 20 mg atorvastatin group(P〈0.05,P〈0.01).The proliferation and adhesion of EPC and the expression level of CD34 in EPC reached their peak on day 60.The expression level of CD133 reached its minimun on day 30.The number of mature EPC decreased more significantly from day 30 in 40mg atorvastatin group than in 20 mg atorvastatin group.The expression level of VEGFR-2kept decreasing from day 60.However,it was significantly higher in 20 mg atorvastatin group than in 40 mg atorvastatin group(P〈0.05,P〈0.01).Conclusion Long-term use of atorvastatin cannot promote the activation of EPC and the formation of blood vessels,and 20 mg atorvastatin can repair vascular intima better than 40 mg atorvastatin.
出处
《中华老年心脑血管病杂志》
CAS
2015年第11期1171-1174,共4页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
广西壮族自治区卫计委科研基金(Z2014546)
关键词
冠心病
干细胞
细胞增殖
血管内膜
降血脂药
coronary disease
stem cells
cell proliferation
tunica intima
antilipemic agents
作者简介
通信作者:杨进,E-mail:lzyangjin@163.com