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机构地区:[1]解放军总医院老年心血管病研究所 [2]北京大学医学部心血管病研究所,北京市100038
出 处:《中国康复理论与实践》2004年第5期271-273,F003,共4页Chinese Journal of Rehabilitation Theory and Practice
摘 要:目的探讨刺激生理状态及过表达的血管平滑肌细胞 β2 肾上腺能受体 (VSMCβ2 AR)对细胞凋亡的影响。方法应用腺病毒介导的转基因技术过表达VSMCβ2 AR ,采用Hoechst 3 3 3 42染色和流式细胞仪分析生理状态下和 β2 AR过表达活化后细胞凋亡情况。结果应用异丙基肾上腺素刺激VSMCβ2 AR 2 4h后 ,流式细胞仪检测存活VSMC数量与对照组相比较并无明显减少 ,48h后较对照组明显减少 (P <0 0 1) ;过表达 β2 AR的VSMC应用异丙基肾上腺素刺激 2 4h后 ,流式细胞仪检测细胞存活率明显下降(P <0 0 1) ,Hoechst染色显示凋亡细胞率明显升高 (P <0 0 1)。结论刺激生理状态及过表达的VSMCβ2 AR具有促进凋亡的效应。ObjectiveTo investigate the effect of β-adrenergic receptor(β 2AR) stimulation on vascular smooth muscle cell apoptosis in physiological state and receptor overexpression model.Methodsβ 2AR overexpression model was established by transgenic techniques. Hoechst 33342 staining as well as flow cytometer(FCM) detected were chosen to measure the incidence of vascular smooth muscle cell apoptosis.ResultsVascular smooth muscle cell exhibited significantly fewer viable cell rate when stimulated with β 2AR agonist isoproteronol for 48 hours compared with control ( P <0.01),while no difference at the time point of 24 hours. Much fewer viable rate detected by FCM and high apoptotic rate by Hoechst staining were observed when VSMCs overexpressing β 2AR were stimulated with isoproteronol for 24 hours ( P <0.01).ConclusionStimulation of physiological and overexpressing β 2AR could induce apoptosis of vascular smooth muscle cell.
分 类 号:R543[医药卫生—心血管疾病]
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