Objective: Use three modeling techniques to establish a mouse model of primary liver cancer and compare its advantages and disadvantages?
Method: 80 14-16 day old C57BL/6 male mice were randomly divided into 4 groups (low-dose DEN group). , High-dose DEN group, DEN+CCl4 group, control group): mice in the low-dose DEN group were intraperitoneally injected with 25mg/kg diethylnitrosamine (DEN), and in the high-dose DEN group, mice were injected intraperitoneally with 40mg/kg. Mice in the DEN+CCl4 group were injected intraperitoneally with 2mg/kg DEN at kg concentration, and 20μl carbon tetrachloride (CCl4) was given 2 weeks later. The dose of intraperitoneal administration was 5 mL/kg, twice a week, for 16 weeks; the control group was not treated? The survival rate of the mice in each group was counted, and the mice in each group were anesthetized and cut off at the 24th week. Model. After execution, the liver was dissected to detect the appearance of the liver, the number of tumors and the incidence of tumors between groups, as well as alanine aminotransferase (ALT), aspartate aminotransferase (AST), Gordi aminotransferase, and glycoprotein 73 (Golgiprotein73) , GP73) and alpha-fetoprotein (AFP) levels?
Results: ALT(P?AFP(Pu003c0.01)? The incidence of tumors in the 3 experimental groups compared with the control group (Pu003c0.001) and tumor count increased significantly (Pu003c0.001))? 24 weeks after modeling, The mortality of mice in the low-dose DEN group was 15? The incidence of liver cancer was 35? The mortality of mice in the high-dose DEN group was 30? The incidence of liver cancer was 86? The DEN+CCl4 group was 20? The incidence of liver cancer 56? All survive, no abnormalities in the liver?
Conclusion: The modeling methods of each experimental group have successfully modeled mouse liver cancer, but the high-dose DEN group has obvious advantages, and whether the incidence and stability of mouse primary liver cancer models provide a new model for mouse liver cancer modeling way?