Ma Rumeng, Li Xiaojing, Kong Fanjun, Ma Jin, Ma Zhe, Zhao Zuoqing, Wen Zhihong, Li Xinhong, Hu Wendong
Department of Surgery, Tangdu Hospital, Fourth Military Medical University 569 Xinsi Road, Xi'an 710038, China.
Department of Aerospace Medical Equipment, Faculty of Aerospace Medicine, Fourth Military Medical University 169 Changle West Road, Xi'an 710032, China.
Int J Clin Exp Pathol. 2015 Jan 1;8(1):497-503. eCollection 2015.
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.
我们建立了兔VX2细胞肝癌模型，以评估缺血再灌注（IR）对活性氧（ROS）生成及肝细胞凋亡率的影响。
36只兔分为对照组（n = 6）和VX2肝细胞癌（HCC）模型组（n = 30），模型组兔肝脏注射VX2细胞悬液。30只HCC兔中，6只作为未进行肝缺血的对照，其余兔采用肝动脉和门静脉夹闭60分钟。再灌注1小时、1天、3天和7天时，处死6只兔，比较肿瘤组织、肿瘤周围正常肝组织及对照组中过氧化氢酶（CAT）和超氧化物歧化酶（SOD）活性的变化以及通过TUNEL法检测的凋亡率。
所有处理动物均发生肝肿瘤。再灌注1小时后，两种组织中的CAT活性均升高（P < 0.05），再灌注1天后肝癌细胞中的CAT活性降至低水平（P < 0.01），但在第3天时升高至高于对照组的水平（P < 0.05）。两种组织中的SOD活性在再灌注后1天前均显著降低，肝癌细胞中的SOD活性在第7天前一直维持在低水平（P < 0.05）。IR后肿瘤组织的凋亡率比正常肝组织增加得更多（P < 0.01）。
向兔肝实质内注射VX2肿瘤细胞悬液在建立肝肿瘤模型方面取得了良好效果。IR通过ROS生成诱导肿瘤组织和正常肝组织凋亡。
