目的　建立化疗药物丝裂霉素诱导肝癌细胞凋亡的模型 ,初步探讨在该凋亡过程中重要凋亡相关基因p5 3和bcl 2的调控作用。方法　用丝裂霉素诱导人肝癌细胞系HepG2 凋亡 ,荧光显微镜和透射电镜观察肝癌细胞的形态学改变 ,琼脂糖凝胶电泳检测凋亡细胞DNA片段的梯状条带 ,用流式细胞仪免疫荧光法检测凋亡不同时期P5 3和Bcl 2蛋白的表达量。结果　 8mg/ml丝裂霉素作用 12 ,2 4,48h后 ,P5 3蛋白表达量明显增高 ,尤以 12h明显 ,而后逐渐下降。Bcl 2蛋白在整个凋亡过程中无明显变化。结论　在化疗药物丝裂霉素诱导肝癌细胞凋亡过程中 ,p5 3基因参与了调控 ,并为凋亡信号传导途径中的早期事件。丝裂霉素诱导的肝癌细胞凋亡途径为p5 3依赖方式 ,而在该凋亡过程中 ,bcl 2基因的调控并不重要。 Objective To establish a model of apoptosis induced by chemotherapeutic drug mitomycin in hepatocellular carcinoma cells, and to explore the regulation of apoptosis-related genes p53 and bcl2 in the process of apoptosis. Methods The apoptosis of HepG2 cells was induced by mitomycin C. The morphological changes of hepatocellular carcinoma cells were observed by fluorescence microscope and transmission electron microscope. The ladders of apoptotic cells DNA fragments were detected by agarose gel electrophoresis. The flow cytometer was used. Immunofluorescence was used to detect the expression of P53 and Bcl-2 at different stages of apoptosis. RESULTS: After 8 mg/ml mitomycin treatment for 12, 24 h, P5 3 protein expression was significantly increased, especially at 12 h, and then gradually decreased. Bcl 2 protein did not change significantly during the whole process of apoptosis. Conclusion During the apoptosis of hepatoma cells induced by chemotherapeutic drug mitomycin C, the p53 gene is involved in the regulation and is an early event in the apoptotic signaling pathway. The mitomycin-induced hepatoma cell apoptosis pathway is p53-dependent, and during this apoptotic process, the regulation of the bcl 2 gene is not important.