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目的研究新城疫病毒弱毒株致Hep-2肿瘤细胞死亡方式及其作用机制。方法应用AO/EB染色、电子显微镜观察、DCFA染色测定细胞内活性氧水平及罗丹明123染色法测定细胞线粒体膜电位等方法分析新城疫病毒弱毒株致Hep-2肿瘤细胞的死亡方式及途径。结果新城疫病毒弱毒株感染能够导致Hep-2肿瘤细胞浓缩,被AO/EB浓染,细胞核缩小,染色质边集。FACS细胞周期分析显示,感染后的Hep-2肿瘤细胞72 h出现二倍体亚峰,G1期细胞凋亡率为8.59%,电子显微镜观察显示,肿瘤细胞核染色质边集、浓缩,细胞核呈固缩状,呈现典型的凋亡形态。另外,细胞内活性氧水平上升,线粒体膜电位下降。结论新城疫病毒弱毒株主要通过细胞内线粒体途径诱导肿瘤细胞凋亡,从而发挥其抑瘤作用。
Objective To study the death mode and mechanism of Hep-2 tumor cells caused by attenuated Newcastle disease virus (NDV) strains. Methods The death pattern and pathways of Hep-2 tumor cells induced by Newcastle disease virus (NDV) attenuated strain were analyzed by AO / EB staining, electron microscopy, DCFA staining and intracellular ROS detection by rhodamine 123 staining. Results The infection of Newcastle disease virus attenuated strains resulted in the concentration of Hep-2 tumor cells, the concentration of AO / EB, the shrinking of nucleus, and the chromatin margination. FACS analysis of cell cycle showed that the infected Hep-2 tumor cells showed diploid sub-peak at 72 h, the rate of apoptosis in G1 phase was 8.59%. Electron microscopy showed that the nuclei of tumor cells were condensed and the nuclei were solidified Shrinkage, showing a typical apoptotic morphology. In addition, intracellular levels of reactive oxygen species increased, mitochondrial membrane potential decreased. Conclusion The attenuated Newcastle disease virus strain induces tumor cell apoptosis mainly through the mitochondrial pathway in the cell and thus exerts its antitumor effect.