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目的 探讨野生型p5 3基因与心肌细胞凋亡的关系及其可能的发生机制。方法 把野生型p5 3基因重组腺病毒转入体外培养的心肌细胞中 ,采用流式细胞计数仪 (FCM) ,透射电镜等实验方法检测细胞凋亡并分析其作用机制。结果 重组腺病毒能有效地将p5 3基因转入心肌细胞中 ;转入的p5 3基因可以导致心肌细胞体积变小、胞浆浓缩、核固缩、染色质边集 ,引起细胞G1期阻滞。结论 野生型p5 3基因可以导致心肌细胞凋亡 ,并能影响细胞周期。以上结果为进一步研究心肌疾病的发病机制及其治疗提供了重要的实验依据。
Objective To investigate the relationship between wild-type p53 gene and cardiomyocyte apoptosis and its possible mechanism. Methods The wild type p5 3 recombinant adenovirus was transfected into cardiomyocytes cultured in vitro. The apoptosis of the cells was detected by flow cytometry (FCM) and transmission electron microscopy (TEM). Results The recombinant adenovirus could efficiently transfer p5 3 gene into cardiomyocytes. The transfected p5 3 gene resulted in the decrease of cardiomyocytes volume, cytoplasm concentration, nuclear pyknosis and chromatin margination, leading to cell arrest in G1 phase . Conclusion The wild type p53 gene can induce cardiomyocyte apoptosis and affect the cell cycle. These results provide an important experimental basis for further study of the pathogenesis of myocardial disease and its treatment.