Experimental Study Of COP1Expression Change In The Process Of Cirrhosis Of The Liver With Hepatocellular Carcinoma

Objective:To study the COP1expression in the liver cirrhosis and liver cancer, indicating that the variation of COP1in the expression level of liver cirrhosis and liver cancer; formation process variation and clinical significance of COP1expression levels in the development of cirrhosis and hepatocellular carcinoma.Methods:90SD rats were fed for one week, according to the randomization principle divided into two groups, the control group, the experimental group. Prior to administration in the control group and the experimental group were randomly selected five to be put to death, the application of the experimental group [1]Diethylnitrosamine and microcystin mouse liver cancer model:every5days by intraperitoneal injection of0.25%DEN solution (10mg/kg)+microcystins MC-LR (20ug/kg) for16weeks, four weeks of carcinogenesis, liver cell injury of liver cell proliferation-hardening of8-12weeks, hepatocellular carcinoma of16weeks.Control group every5days by intraperitoneal injection of normal saline. Before each injection to measure the weight of the rats injected dose be adjusted according to changes in body weight and general condition, if abnormal timely disable or suspend given DEN, to reduce mortality. The control group and the experimental group were fed with standard rat chow throughout the experiment lasted17weeks.4weeks after the experiment,8and12weeks, respectively, in the control group and the experimental group were randomly selected10were killed and the remaining rats of the control group and the experimental group were sacrificed at16weeks.(Visual experimental animal deaths minor adjustment).Results:1. Experimental rats liver specimens paraffin HE staining: liver cell injury of liver cell proliferation-hardening of hepatocellular carcinoma period.2.PCR detection COP1expression first decreased and then abruptly increase COP1expression in the liver cell injury midterm difference, p <0.05.-Hardening of no significant difference, p>0.05, significant difference in hepatocellular carcinoma (p<0.05) in the liver cell proliferation. Liver cell injury COP1expression were lower than the control group difference, p<0.05; hepatocellular carcinoma formation COP1expression was significantly higher, p<0.05.3. Immunohistochemical results are shown:in the high expression status of p53in the process of liver damage, liver cell injury of p53expression upward trend, and there is a significant difference P<0.05, cirrhosis of p53expression compared with hepatic fibrosis formation of a slight decrease in but no statistically significant p>0.05, hepatocellular carcinoma formation of p53upregulation, significant differences p<0.05compared to the formation of cirrhosis. Experimental group of p53expression were higher and the difference is significant, p<0.05.Conclusion:1.COP1basis liver pathological changes in the expression also changed.2.Indicates that cirrhosis of the liver may be combined incidence of hepatocellular carcinoma in cirrhosis COP1upregulation.3.The expression of COP1regular changes in liver cirrhosis and the combined liver cancer process appears to COP1predictors of cirrhosis with liver cancer...