The protective effect of Nrf2 antioxidant pathway in the acute liver injury induced by CCl4 in rats

  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 in each group, and another 10 male Wistar rats were selected. The transgenic rats were microinjected into male pronucleus through the carrier, and the target gene Nrf2 was obtained. -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 the Nrf2-tk integration group were given intravenously 1% polysorbate-80 for 4 days, and 1% polysorbate-80 was given on the fourth day. After 30 minutes, 7.5 mg/kg CCl4 was administered intravenously, and the rats were sacrificed 24 hours later. Measure the level of AST, ALT and LDH in serum, measure the content of MDA, GSH, GSSG in liver tissue, and calculate the ratio of GSH/GSSG. The liver tissues were collected, routinely embedded in paraffin, stained with HE, and the pathological changes of liver tissues were observed under an optical microscope.

  Results: Compared with the solvent control group, the serum AST, ALT and LDH levels of rats in the CCl4 group were significantly increased (P<0.05), and="" the="" levels="" of="" alt="" ldh="" in="" nrf2-tk="" transgenic="" rats="" were="" also="" mild="" but="" difference="" was="" not="" statistically="" significant="" p="">0.05). The liver MDA content and the GSH/GSSG ratio show that the Nrf2-tk integrated group can effectively reduce the lipid peroxidation damage caused by CCl4 and the consumption of glutathione. The liver pathological observation results show that compared with the CCl4 group, the Nrf2-tk integrated group Significantly reduce the damage caused by CCl4.

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