动物造模,慢性肝损伤 z-bio 2022-01-11 220

　　Objective To investigate the antioxidant protective effect of teretin on CCl4-induced chronic liver injury in mice.

　　Methods The mice were randomly divided into the normal group, the model group, the turtle peptide group (50, 100, 200 mg/kg) and the positive drug group. The mice in the normal group were given normal saline, and the mice in the turtle peptide group were given different doses of turtle peptide every day. The mice in the positive drug group were intraperitoneally injected with silymarin (100 mg/kg) every day for 6 consecutive weeks. At the same time, except the normal group mice were intraperitoneally injected with peanut oil solution, the other groups were intraperitoneally injected with 0.1% CCl4 peanut oil solution 10 mL/kg, each 2 times a week for 6 consecutive weeks, 24 h after the last administration, the mice were weighed and sacrificed to get liver tissue, HE staining was used to observe the changes of liver histology, and spectrophotometry was used to detect liver function enzymes (AST, ALT), antioxidant enzymes (SOD, CAT, GSH-Px), peroxide (MDA), fluorescence quantitative PCR method was used to determine the gene expression of inflammatory factors, apoptosis factors and fibrosis factors, and ELISA was used to determine the protein levels of inflammatory factors.

　　Results Microscopic observation showed that there was no abnormality in the liver cells of the mice in the normal group. The liver cells of the mice in the model group showed congestion, necrosis, fibrosis, and the disappearance of hepatic lobules. The degree of cell damage was significantly weakened, and the liver and spleen index of the mice was significantly lower than that of the model group. Compared with the model group, the activities of AST and ALT in the serum of the mice in the turmeric peptide group were significantly reduced, the content of MDA in the liver was significantly reduced, and antioxidant enzymes (SOD, CAT and CAT) were significantly reduced. , GSH-Px) activity was significantly increased, inflammatory factors (IL-6, TNF-α, iNOS) protein and gene expression levels were significantly decreased, pro-apoptotic factors (Bax, Caspase-3) and fibrosis factors (α-SMA) , TGF-β) gene expression was also significantly reduced.

　　CONCLUSION: Dichotomide peptide can effectively improve CCl4-induced chronic liver injury in mice, and its protective effect may be closely related to the antioxidative effect of dichondrite peptide.