粒细胞集落刺激因子动员内皮祖细胞预防再狭窄的研究  被引量:1

Granulocyte colony stimulating factor for prevention of restenosis by accelerating endothelial progenitor cells repair

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作  者:孙智山[1,2] 周胜华[1] 曾建平 黄河 

机构地区:[1]中南大学湘雅二医院,湖南长沙410011 [2]湘潭市中心医院,湖南湘潭411100

出  处:《现代生物医学进展》2010年第18期3430-3433,共4页Progress in Modern Biomedicine

摘  要:目的:观察粒细胞集落刺激因子是否能通过加速内皮修复预防再狭窄,并探讨该作用与其动员效应即EPCs数量和功能变化的相关性。方法:30只SD大鼠随机均分为假手术组、损伤未干预组和G-CSF组,后两组行颈总动脉球囊损造模,G-CSF组连续给药7天后观察各组外周血内皮祖细胞的数量和增值、粘附、迁移功能,4周后观察再狭窄和再内皮化程度。结果:G-CSF组再内皮化率高于对照组,再狭窄率低于对照组,再内皮化率和再狭窄率呈线性负相关;G-CSF组内皮祖细胞数量明显增加,内皮祖细胞增值、粘附、迁移功能也明显提高。结论:G-CSF通过加速内皮修复能预防再狭窄,该作用与其动员效应即内皮祖细胞数量的增加和增值、粘附、迁移功能的提高有关。Objective:To investigate the effects of G-CSF in preventing restenosis by accelerating reendothelialization and the re-lated mechanisms on EPCs quantity and functions.Method:30 SD rats were randomly divided into sham operation grouop,model group and G-CSF group.In the latter two groups each rat's left carotid was injured by balloon.After successive G-CSF administration for 7 days,total mononuclear cells isolated from peripheral blood by density gradient centrifugation were cultured for 7 days.EPCs were char-acterized as adherent cells double positive for Dil-acLDL-uptaking and lectin-binding,and EPCs proliferation,migration and adhesion activities were measured.Four weeks after bollon injury,the intima/media ration and reendotheliaization ration were measured.Results:G-CSF accelerated reendothelialization and alleviated intima/media ratio,meanwhile the EPCs quantity and their proliferation,adhesion and migration activities were significantly elevated.Conclusions:G-CSF can accelerate alleviate restenosis by accelerating reendothelial-ization,and the mechanisms on which relate to a promotion of the quantity and the proliferation,adhesion and migration activities of periphery blood EPCs.

关 键 词:粒细胞集落刺激因子 内皮祖细胞 再狭窄 再内皮化 

分 类 号:R541.4[医药卫生—心血管疾病]

 

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