目的　建立体内、外肝细胞凋亡模型 ,为进一步研究药物对肝细胞凋亡的调控作用奠定基础。方法　 (1)采用D GalN +LPS小鼠腹腔注射建立体内肝细胞损伤模型 ;(2 )采用H2 O2 (0 0 5～ 0 4mmol·L-1)与原代大鼠肝细胞共培养建立体外肝细胞损伤模型 ,分别用形态学、DNA电泳和流式细胞术检测等方法。结果　 (1)D GalN(70 0mg·kg-1,ip) +LPS(1μg·kg-1,ip)可明显升高小鼠血中TNF水平和MDA含量 ,使肝线粒体Mn SOD活性降低 ,小鼠肝细胞皱缩变小、核染色质凝聚和DNA片段化 (DNA梯状条带 ) ;(2 )H2 O2(0 1mmol·L-1,1h)可致大鼠肝细胞增殖受抑、肝细胞MDA含量升高 ,肝细胞DNA的AO荧光染色变亮 ,DNA电泳呈片段化 ,流式细胞术肝细胞DNA亚G1峰 (即凋亡峰 )明显升高。结论　采用D GalN +LPS与低浓度H2 O2 可分别建立较理想的体内、外肝细胞凋亡模型 Objective To establish a hepatocyte apoptosis model in vitro and in vivo, which lays the foundation for further study on the regulation of hepatocyte apoptosis by drugs. Methods (1) In vivo models of hepatocellular injury were established by intraperitoneal injection of D GalN + LPS mice. (2) H 2 O 2 (0 0 5 ~ 0 4 mmol·L -1) was used to establish an in vitro hepatic Cell injury model, respectively, by morphology, DNA electrophoresis and flow cytometry and other methods. Results (1) D GalN (70μg · kg-1, ip) + LPS (1μg · kg-1, ip) could significantly increase the levels of TNF and MDA in blood and decrease the activities of Mn SOD in liver mitochondria (2) H 2 O 2 (0 1 mmol·L-1, 1 h) can inhibit the proliferation of rat hepatocytes, and the hepatic fibrosis Cell MDA content increased, AO staining of DNA in liver cells became bright, and DNA electrophoresis was fragmented. The expression of sub-G1 peak (the peak of apoptosis) of hepatocytes in flow cytometry was significantly increased. Conclusion D GalN + LPS and low concentration of H2O2 can establish a more ideal model of hepatocyte apoptosis in vitro and in vivo