中华老年心脑血管病杂志
中華老年心腦血管病雜誌
중화노년심뇌혈관병잡지
Chinese Journal of Geriatric Heart Brain and Vessel Diseases
2015年
11期
1171-1174
,共4页
刘洁%银剑斌%杨进%吴敏嘉%洪艳俐
劉潔%銀劍斌%楊進%吳敏嘉%洪豔俐
류길%은검빈%양진%오민가%홍염리
冠心病%干细胞%细胞增殖%血管内膜%降血脂药
冠心病%榦細胞%細胞增殖%血管內膜%降血脂藥
관심병%간세포%세포증식%혈관내막%강혈지약
coronary disease%stem cells%cell proliferation%tunica intima%antilipemic agents
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(20 mg )20例及大剂量组(40 mg )20例。所有入选患者于服药前服药5、15、30、60、90和120 d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、M T T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30 d时最强,30 d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60 d时达高峰;CD133在30 d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60 d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。20 mg的阿托伐他汀钙对血管内膜的修复更优于40 m g。
目的:通過人體藥物臨床試驗,觀察不同劑量阿託伐他汀鈣對冠心病患者外週血內皮祖細胞(EPC )增殖、遷移、黏附及血管脩複能力的影響。方法選擇冠心病患者40例,根據服用阿託伐他汀鈣的劑量不同,分為小劑量組(20 mg )20例及大劑量組(40 mg )20例。所有入選患者于服藥前服藥5、15、30、60、90和120 d分彆抽取外週血穫取外週血單箇覈細胞,體外培養後進行細胞染色與鑒定、M T T比色法檢測細胞增殖、檢測EPC的遷移及黏附能力,流式細胞儀分析 EPC標記錶麵CD34、CD133、人血管內皮細胞生長因子受體2(VEGFR‐2)的錶達。結果EPC的遷移能力在30 d時最彊,30 d後大劑量組遷移能力的下降趨勢顯著高于小劑量組( P<0.05,P<0.01);EPC增殖、黏附和CD34的錶達在60 d時達高峰;CD133在30 d時最低,而此後大劑量組成熟EPC的下降率顯著高于小劑量組;VEGFR‐2的細胞錶達在60 d後呈持續下降趨勢,而小劑量組VEGFR‐2明顯高于大劑量組(P<0.05,P<0.01)。結論長期使用阿託伐他汀鈣併不能有效促進EPC的活化及新生血管的生成。20 mg的阿託伐他汀鈣對血管內膜的脩複更優于40 m g。
목적:통과인체약물림상시험,관찰불동제량아탁벌타정개대관심병환자외주혈내피조세포(EPC )증식、천이、점부급혈관수복능력적영향。방법선택관심병환자40례,근거복용아탁벌타정개적제량불동,분위소제량조(20 mg )20례급대제량조(40 mg )20례。소유입선환자우복약전복약5、15、30、60、90화120 d분별추취외주혈획취외주혈단개핵세포,체외배양후진행세포염색여감정、M T T비색법검측세포증식、검측EPC적천이급점부능력,류식세포의분석 EPC표기표면CD34、CD133、인혈관내피세포생장인자수체2(VEGFR‐2)적표체。결과EPC적천이능력재30 d시최강,30 d후대제량조천이능력적하강추세현저고우소제량조( P<0.05,P<0.01);EPC증식、점부화CD34적표체재60 d시체고봉;CD133재30 d시최저,이차후대제량조성숙EPC적하강솔현저고우소제량조;VEGFR‐2적세포표체재60 d후정지속하강추세,이소제량조VEGFR‐2명현고우대제량조(P<0.05,P<0.01)。결론장기사용아탁벌타정개병불능유효촉진EPC적활화급신생혈관적생성。20 mg적아탁벌타정개대혈관내막적수복경우우40 m g。
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 (20 in each group) .Their peripheral mononuclear cells were calculated ,cul‐tured ,and stanined .The proliferation ,adhesion ,migration of EPC were assayed by MTT colori‐metry .Expressions of surface CD34 ,CD133 ,and VEGFR‐2 in EPC were detected by cytometry . Results The migration of EPC reached its peak on day 30 ,and decreased more significantly from day 30 in 40 mg 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 40 mg atorvastatin group than in 20 mg atorvastatin group .The expression level of VEGFR‐2 kept decreasing from day 60 .However ,it was signifi‐cantly 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 forma‐tion of blood vessels ,and 20 mg atorvastatin can repair vascular intima better than 40 mg atorvas‐tatin .