动物造模,急性肝损伤 z-bio 2022-07-21 246

　　Objective: To study the protective effect of Nrf2 oxidative damage pathway in CCl4-induced acute liver injury in rats.

　　METHODS: Twenty male Wistar rats were randomly divided into solvent control group and CCl4 group, 10 rats in each group, and 10 male Wistar rats were selected. The target gene Nrf2 was obtained by microinjection of male pronucleus of transgenic rats through vector. -tk integration and specific expression of transgenic rats, as CCl4 + Nrf2 integration group. The solvent control group was given 1% polysorbate-80 intravenously for 4 days, and the CCl4 group and Nrf2-tk integration group were given 1% polysorbate-80 intravenously for 4 days, and 1% polysorbate-80 was given on the 4th day After 30 min, 7.5 mg/kg CCl4 was administered intravenously, and the rats were sacrificed 24 h later. The levels of AST, ALT and LDH in serum were determined, and the contents of MDA, GSH and GSSG in liver tissue were determined respectively, and the ratio of GSH/GSSG was calculated. The liver tissue was collected, routinely embedded in paraffin, and stained with HE. The pathological changes of the liver tissue were observed under a light microscope.

　　Results: Compared with the solvent control group, the serum levels of AST, ALT and LDH in the CCl4 group were significantly increased (P < 0.05), and the levels of AST, ALT and LDH in the Nrf2-tk transgenic group were also slightly increased. increased, but the difference was not statistically significant (P > 0.05). Liver MDA content and GSH/GSSG ratio showed that Nrf2-tk integration group could effectively reduce lipid peroxidative damage and glutathione consumption caused by CCl4. Liver pathological observation showed that compared with CCl4 group, Nrf2-tk integration group The damage caused by CCl4 was significantly reduced.

　　Conclusion: The Nrf2 antioxidant damage pathway plays an important protective role in CCl4-induced acute liver injury in rats.