三氧化二砷诱导血管平滑肌细胞凋亡机制的研究 |
投稿时间:2010-04-19 点此下载全文 |
引用本文:李慧,张延斌,宋豪,肖菲,张卓奇,李东野.三氧化二砷诱导血管平滑肌细胞凋亡机制的研究[J].医学研究杂志,2010,39(10):78-81 |
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中文摘要:目的探讨三氧化二砷(As2O3)诱导血管平滑肌细胞(VSMCs)凋亡的机制,为其作为药物涂层支架的涂层药物提供理论依据。方法用改良的植块贴壁法体外培养SD大鼠VSMCs,应用MTT法、酶标仪法、流式细胞术等方法观察不同浓度As2O3诱导VSMCs凋亡时裂解液中线粒体跨膜电位(△Ψm) 及半胱天冬蛋白酶-3(caspse-3)活性的变化。结果适宜浓度As2O3诱导VSMCs凋亡时△Ψm明显下降,与对照组相比P<0.05;裂解液中caspse-3酶活性明显增高,与对照组相比,P<005。结论适宜浓度的As2O3可明显促进VSMCs凋亡,其可能机制是降低△Ψm和激活caspse-3酶。 |
中文关键词:血管平滑肌细胞(VSMCs) 三氧化二砷 凋亡 线粒体跨膜电位(△Ψm) caspse-3酶 |
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Study on the Mechanisms of Arsenic Trioxide-induced Vascular Smooth Muscle Cells Apoptosis in vitro |
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Abstract:ObjectiveTo discuss the mechanism of As2O3-induced vascular smooth muscle cells (VSMCs) apoptosis and provide theoretical basis for the use of As2O3 in drug-eluting stents in future. MethodsVSMCs of SD rats were cultured in vitro by modified tissue explants-attached method. NBT reduction test, enzyme-labeling instrument and flow cytometry (FCM) were applied to observe the alteration of mitochondrial membrane potential (△Ψm) and activity of caspase-3 when VSMCs apoptosis was induced by different dosage of As2O3. ResultsThe mitochondrial transmembrane potential obviously decreased and the caspase-3 activity obviously increased when VSMCs apoptosis was induced by appropriate dosage of As2O3 (P<0.05) as compared with control group. ConclusionAs2O3 of appropriate dosage can obviously promote apoptosis of VSMCs and the mechanism may be decreasing mitochondrial transmembrane potential and activating caspase-3. |
keywords:Vascular smooth muscle cells (VSMCs) Arsenic trioxide Apoptosis Mitochondrial transmembrane potential Caspase-3 |
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