Effect of ischemia reperfusion on rabbit VX2 cells in a hepatocellular carcinoma model

We established a rabbit VX2 cell liver carcinoma model to evaluate effects of ischemia reperfusion (IR) on reactive oxygen species (ROS) development and liver cell apoptosis rates.

Thirty-six rabbits were divided into a control (n=6) and a VX2 hepatocellular carcinoma (HCC) model group (n=30), which received VX2 cell suspension injections into their livers. From the 30 HCC rabbits, 6 rabbits served as control without hepatic ischemia and the rest were treated with hepatic artery and portal vein clamps for 60 minutes. At 1 hour, 1 day, 3 days and 7 days of reperfusion, 6 rabbits were sacrificed and changes of catalase (CAT) and super-oxide dismutase (SOD) activities as well as apoptosis rates, measured by TUNEL assays, were compared between tumor tissues, normal tumor surrounding hepatic tissues and controls.

All treated animals developed liver tumors. The CAT activity increased in both tissues 1 hour after reperfusion (P < 0.05) and dropped to low levels in the hepatocarcinoma cells at day 1 after reperfusion (P < 0.01), but increased to higher levels than the control on day 3 (P < 0.05). SOD activity decreased significantly in both tissues until day 1 after reperfusion and kept low in the hepatocarcinoma cells until day 7 (P < 0.05). The apoptosis rates after IR increased more in cancer than in normal hepatic tissues (P < 0.01).

Injection of VX2 tumor cell suspension into rabbit liver parenchyma achieved good results for creating a liver tumor model. IR induced apoptosis of tumor tissue and normal hepatic tissues via ROS development.