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作 者:汪艳[1] 易有荣[2] 崔冶建[2] 董长垣[1]
机构地区:[1]武汉大学医学院病毒学国家重点实验室,武汉430071 [2]武汉大学医学结构生物学研究中心,武汉430071
出 处:《武汉大学学报(医学版)》2006年第4期425-428,F0002,共5页Medical Journal of Wuhan University
基 金:国家自然科学基金资助项目(编号:30271471)
摘 要:目的:探讨BTV-HbC3对人肝癌Hep-3B细胞线粒体功能和膜电位的影响及其与细胞凋亡关系。方法:利用透射电镜和荧光显微镜观察Hep-3B细胞感染BTV-HbC3在24,36,48 h的凋亡情况与其线粒体形态变化;噻唑蓝(MTT)法检测其线粒体功能;流式细胞仪检测经Rh123/PI染色的BTV-HbC3诱导该细胞线粒体跨膜电位(△Ψm)和Annexin V/PI染色的细胞凋亡率。结果:Hep-3B细胞感染病毒在24,36,48 h时可导致线粒体功能下降,同时使线粒体膜电位显著降低,细胞凋亡率显著增加。结论:BTV-HbC3通过诱导凋亡来抑制人肝癌细胞的生长,其机制与线粒体跨膜电位下降有关。Objective: To explore the changes of in human hepatic carcinoma cells Hep-3B after bluetongue virus HbC3 (BTV-HbC3) infection and their relationship with the BTV-HbC3 induced apoptosis. Methods. Morphological changes of apoptosis and mitochondria of Hep-3B cells infected with BTV-HbC3 were observed under fluorescence microscope and transmission electron microscope. Mitochondrial function was assessed with MTT. The mitochondrial transmembrane potential of Hep-3B cells straining Rh123/PI and the apoptosis of Hep-3B cell staining Annexin V/PI were measured by flow cytometry (FCM). Results: Mitochondrial transmembrane potential and mitochondrial function of Hep-3B cells were significantly decreased at 24, 36 and 48 hours after infection, but the rate of Hep-3B cells apoptosis markedly increased. Conclusion: BTV-HbC3 might inhibit the Hep-3B cells growth by inducing apoptosis and its mechanism might be related to the loss of △Ψm.
关 键 词:蓝舌病毒HbC3 细胞凋亡 线粒体 膜电位 人肝癌细胞
分 类 号:R373.1[医药卫生—病原生物学]
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