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目的：探讨肝癌发生过程中细胞周期调控下细胞增殖与凋亡的关系。方法：以二乙基亚硝胺（ ＤＥＮ） 诱导的大鼠实验性肝癌为模型，以Ｋｉ６７ 抗原和ＳｕｂＧ１ 法分别作为细胞增殖和细胞凋亡定量分析方法。凋亡细胞比例（Ａｐ） 与Ｋｉ６７ 阳性细胞比例（Ｋｉ） 之比值（Ａｐ／Ｋｉ） 为描述两者关系的客观指标。结果：除诱癌８ 周和２０ 周外，余各实验组的细胞凋亡数目与对照组相比均存在明显差异（Ｐ＜ ０－０５） 。在肝硬变前期和肝硬变期Ａｐ 与Ｋｉ 基本呈正比关系。Ａｐ／Ｋｉ 于诱癌２ 、１０ 、１８ 周较高，峰值位于诱癌２ 周。结论：①大鼠肝癌发生过程中，机体进行细胞增殖以补偿因ＤＥＮ损害导致肝细胞减少的同时，还通过细胞周期调控机制，以细胞凋亡为表现形式，始终在监测和清除着异常细胞；②肝硬变前期和肝硬变期，机体通过细胞凋亡，使组织增生的速度和规模受到控制。
Objective: To investigate the relationship between cell proliferation and apoptosis in the process of hepatocarcinogenesis. METHODS: Rat liver cancer model induced by diethylnitrosamine (DEN) was used as a model, and Ki67 antigen and SubG1 method were used as quantitative methods for cell proliferation and apoptosis, respectively. The ratio of apoptotic cell ratio (Ap) to Ki-67 positive cell ratio (Ki) (Ap/Ki) is an objective index to describe the relationship between the two. Results: Except for 8 weeks and 20 weeks of cancer induction, there was a significant difference in the number of apoptotic cells in the experimental groups compared with the control group (P < 0-05). In the liver cirrhosis and liver cirrhosis, Ap is basically proportional to Ki. Ap/Ki was more likely to induce cancer at 2, 10, and 18 weeks, with a peak at 2 weeks of induction. Conclusion: 1 During the development of rat hepatoma, the body carries out cell proliferation to compensate for the decrease of hepatocytes due to DEN damage. At the same time, it also monitors and clears abnormal cells through the cell cycle regulation mechanism and the manifestation of apoptosis. 2 In the early stages of cirrhosis and cirrhosis, the body undergoes apoptosis, which controls the rate and scale of tissue proliferation.