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作 者:周永兰[1] 陈清枝[2] 张延斌[2] 王人彭[1] 张义勤[1] 骆秉辁[1]
机构地区:[1]江苏大学附属医院徐州市第三人民医院心内科,江苏徐州221005 [2]徐州医学院附属医院心内科
出 处:《临床心血管病杂志》2007年第4期301-303,共3页Journal of Clinical Cardiology
摘 要:目的探讨17β雌二醇(E2)对血管平滑肌细胞(VSMC)凋亡的影响及其可能机制。方法应用流式细胞仪检测低、高浓度17βE2(10、100nmol/L)对传代的VSMC凋亡率的影响,并通过细胞免疫组化方法观察对凋亡相关基因c-myc表达的影响。结果17βE2作用下VSMC凋亡率显著高于对照组(P<0.01),伴随着VSMC凋亡率的增加,c-myc蛋白的表达亦增强,且表现明显的浓度依赖性。结论17βE2具有诱导VSMC凋亡的作用,其部分机制可能是通过上调促凋亡基因c-myc的表达有关。Objective:To investigate the effects of 17β estradiol (17β-E2) on apoptosis of vascular smooth muscle cells (VSMC) and the possible underlying mechanism. Method: The apoptosis was examined by flow cytometry in subcultured VSMC exposed to different concentrations (10, 100 nmol/L)of 17β-E2. The intracellular localization of c-myc protein in VSMC was detected by immunocytochemical method. Result: The ratio of VSMCs apoptosis was increased significantly by 17β-E2 with dose-dependant compared with control group(P〈0.01), as accompanied by a significant raise of pro-apoptosis c-myc protein expression. Conclusion: 17β-E2 might induce the apoptosis of VSMC in part by the reason that the expression of pro-apoptosis oncogene c-myc protein upregulates.
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