动物实验,Nrf2抗氧化 z-bo 2020-08-24 587

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

　　Method: 20 male Wistar rats were randomly divided into solvent control group and CCl4 group, each group selected 10 male Wistar rats and 10 male Wistar rats, and the male pronucleus of transgenic rats was used as a carrier. This goal is achieved through microinjection. Transgenic rats with gene Nrf2-tk integration and specific expression were used as the CCl4 + rf2 integration group. The vehicle control group received 1% polysorbate 80 intravenously for 4 days, the CCl4 group and the Nrf2-tk combination group received intravenous injection of 1% polysorbate 80 for 4 days, and received 1% polysorbate 8030 on the fourth day for a few minutes . 7.5 mg/kg CCl4 was administered intravenously, and the rats were sacrificed 24 hours later. Measure the levels of AST, ALT and LDH in serum, measure the contents of MDA, GSH and GSSG in liver tissue, and calculate the GSH/GSSG ratio. Collect liver tissues, routinely embed them in paraffin, stain with HE, and observe pathological changes in liver tissues by optical microscope.

　　Result: Compared with the vehicle control group, the serum AST, ALT and LDH levels of rats in the CCl4 group were significantly increased (P0.05). The liver MDA content and GSH/GSSG ratio indicated that the Nrf2-tk integrated group can effectively reduce the lipid peroxidation damage and glutathione consumption caused by CCl4. Pathological observations in the liver showed that the Nrf2-tk integration group was compared with the CCl4 group. Greatly reduce the damage of CCl4.

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