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机构地区:[1]湘潭市中心医院,湖南湘潭411100 [2]中南大学湘雅二医院,湖南长沙411011
出 处:《现代生物医学进展》2012年第35期6871-6873,共3页Progress in Modern Biomedicine
基 金:国家自然科学基金项目(30871053)
摘 要:目的:观察他汀对冠心病患者内皮祖细胞(EPCs)增殖力的影响及与PI3/Akt和ERK信号通道的相关性。方法:冠心病和非冠心病患者各16例纳入实验,非冠心病患者的10mL外周血来源的单个核细胞纳入正常组,冠心病患者的40mL外周血来源的单个核细胞均分纳入10μmol/L阿托伐他汀组、10μmol/L阿托伐他汀+PI3/Akt通道阻滞剂LY294002组和10μmol/L阿托伐他汀+ERK信号通道阻滞剂PD98059组,均向EPCs方向分化,以VEGFR2、CD34和AC133流式鉴定;观察冠心病患者EPCs增殖力的变化及他汀的影响,观察LY294002和PD98059分别阻断PI3/Akt和ERK通道后他汀对冠心病患者EPCs增殖力作用的变化。结果:与非冠心病人对比,冠心病患者EPCs的增殖(0.23±0.02 to 0.14±0.02,P<0.001)功能下降,阿托伐他汀明显提高冠心病患者EPCs的增殖力(0.14±0.02 to 0.20±0.02,P<0.05);该作用可为PI3/Akt通道阻滞剂LY294002阻断(0.20±0.02 to 0.16±0.02,P<0.001),但ERK信号通道阻滞剂PD98059无此作用(0.20±0.02比0.20±0.02,P>0.05)。结论:阿托伐他汀可通过PI3/Akt通道而非ERK信号通道上调冠心病患者外周血来源EPCs的增殖力。Objective: To study the effects of statin on the proliferation function of EPCs isolated from CHD patients and the related mechanisms on PI3/Akt and ERK signaling pathway.Methods: 16 CHD patients and 16 matched control subjects were enrolled.Total mononuclear cells isolated from 10 ml peripheral blood of control subjects were enrolled in normal groups,and the total mononuclear cells isolated from 40 ml peripheral blood of CHD patients were evenly divided into four group: CHD group,10μmol/L atrovastatin group,10μmol/L atrovastatin plus 10μmol/L LY294002 group,and 10μmol/L atrovastatin plus 10μmol/L PD98059 group,Then the cells were cultured toward EPCs which were characterized as cells positive for VEGFR2,CD34 and AC133 expression.The EPCs proliferation function measured by MTT assay of CHD patients was compared with normal subjects.The impacts of atrovastatin on the proliferation function of EPCs from CHD patients were observed,and the blocking effects of LY294002 and PD98059 on which were observed.Results: Compared with normal subjects,the proliferation 0.23±0.02 to 0.14±0.02,P0.001) function of EPCs of CHD patients were impaired.Atrovastatin significantly improved EPCs' proliferating(0.14±0.02 to 0.20±0.02,P0.05) function;Treated with LY294002,The effects of atrovastatin on EPCs' proliferation were blocked by LY294002(0.20±0.02 to 0.16±0.02,P0.001)other than PD98059(0.20±0.02 to 0.20±0.02,P0.05).Conclusion: Atrovastatin elevate EPCs' proliferation function of CHD patients via PI3/Akt other than ERK signaling pathway.
分 类 号:R541.4[医药卫生—心血管疾病]
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