Screening for Protective Effect Target of Deproteinized Extract of Calf Blood and Its Mechanisms in Mice with CCl4-Induced Acute Liver Injury. Mus musculus

Liver injury is the common pathological basis of various liver diseases, and its existence for a long time is often a important initiation factor to lead to liver fibrosis, and even liver cirrhosis and hepatocellular carcinoma (HCC), so that the prevention and treatment of liver injury is one of the key links in the clinical therapy of liver diseases, and the timely control of the occurrence and development of liver injury will have an important clinical significance in the treatment of liver disorders. It has been reported that deproteinized extract of calf blood (DECB) can inhibit the replication of hepatitis B virus and has a protective effect on the liver function after a traumatic liver injury. However, there are few studies on the regulatory factors and mechanisms of DECB effects. In this study, an acute mouse liver injury model was established with carbon tetrachloride (CCl4), mRNA expression microarray was used to screen the differentially expressed genes and related pathways in mice in the DECB group and model group, and the target of protective effect of DECB and its related mechanism were found in mice with acute liver injury induced by carbon tetrachloride, which may provide an important theoretical basis for the further research and development of DECB. Overall design: After they were acclimated to the laboratory environment for 3d, 20 male mice were randomly divided into 2 groups: model group (M), DECB group, 10 mice in each group.The DECB group was given DECB (1g/kg), and those in the M group (20 BW) were given normal saline (20mL/kg) intragastrically once daily continuously for 30d. At two hours after the last administration, mice in M and DECB groups were injected with 10% carbon tetrachloride blend oil (10mL/kg).