替格瑞洛拮抗ADP抑制的内皮细胞小管形成  

Effect of ticagrelor on inhibited tubulogenesis induced by ADP in endothelial cells

作　　者：吴浩鑫 黄至斌[1] 卢贵华[1] 王业松[1] 

机构地区：[1]中山大学附属第一医院心内科,广东广州510080

出　　处：《热带医学杂志》2017年第2期161-165,共5页Journal of Tropical Medicine

基　　金：广东省科技计划(2013B021800118)

摘　　要：目的研究体外实验中抗血小板药物替格瑞洛对二磷酸腺苷(ADP)诱导的人脐静脉内皮细胞(HUVECs)小管形成的影响。方法用CCK8实验探索替格瑞洛作用于内皮细胞的最大合适浓度及细胞增殖情况。以小管形成实验观察不同浓度的ADPβS和替格瑞洛对内皮小管形成的影响,Western blot检测内皮细胞p AKT的表达情况。结果替格瑞洛可浓度依赖性的促进HUVECs的增殖(P<0.05),有效阻断ADPβS对内皮细胞增殖的抑制作用,上调p AKT信号通路(P<0.05),同时显著的逆转ADPβS所诱导的小管抑制(P<0.05)。结论替格瑞洛可拮抗ADP抑制的内皮细胞小管形成,为冠心病血管新生提供新的研究思路以及治疗策略。Objective To study the effect of ticagrelor,a new antiplatelet agent,on inhibited tubulogenesis induced by ADP in human umbilical vein endothelial cells（HUVECs）in vitro. Methods The optimal concentration and cell proliferation of endothelial cells were determined by CCK8 assay. Endothelial tubulogenesis was induced by different concentrations of ADPβS and ticagrelor,and the expression of p AKT was detected by Western blot. Results Ticagrelor could promote the proliferation of HUVECs in a concentration-dependent manner（P〈0.05）. Moreover,it could effectively reverse the blood vessel inhibition caused by ADPβS, and increase the expression of p AKT（P〈0.05） and tubulogenesis（P〈0.05）.Conclusion Ticagrelor may directly reversed the inhibition of tubulogenesis by ADP,which providing new therapeutic perspectives for angiogenesis of coronary heart disease.

关 键 词：替格瑞洛 二磷酸腺苷 小管形成 冠心病 内皮细胞 

分 类 号：R541.4[医药卫生—心血管疾病]