动物造模 中国实验动物信息网 2023-06-13 796

　　Objective To investigate the damage of acrylamide to mouse lung tissue and its possible mechanism.

　　Method: 4-week-old SPF grade male mice were used as experimental animals and randomly divided into a control group and an ACR group (10mg/(kg · d) and 20mg/(kg · d), with 8 mice in each group. The control group was given regular drinking water; The ACR group was prepared with mice drinking 5mL of water daily to determine the concentration of ACR exposure, which was replaced every 3 days and treated continuously for 4 weeks. After the experiment, lung tissue was taken and sliced for histopathological analysis; Using a reagent kit to detect relevant indicators of oxidative damage; Further use immunofluorescence and Western Blot techniques to detect the expression of Nrf2 ⁃ ARE pathway related proteins.

　　Compared with the control group, the body weight of mice gradually decreased with the increase of ACR intake concentration (P<0.01); Histopathological analysis revealed that the lung tissue of mice in the ACR group exhibited bronchial epithelial hypertrophy, alveolar epithelial hyperplasia, and a significant reduction in alveolar space area. The pathological changes were more pronounced in the 20mg/(kg · d) group; The detection of oxidative stress indicators found that compared with the control group, the GSH PX activity in lung tissue gradually decreased with the increase of ACR intake concentration (P<0.05); The vitality gradually decreased (P<0.05); The vitality gradually decreased (P<0.01); The content of MDA significantly increased (P<0.01); The immunofluorescence results showed that compared with the control group, the expression of Nrf2 protein in the lung tissue of the ACR group significantly increased, with the highest expression in the 10mg/(kg · d) group (P<0.001); And there was nuclear translocation phenomenon, with a significant decrease in the expression of its companion protein Keap1, with the lowest expression in the 10mg/(kg · d) group (P<0.001); Western Blot results showed that compared with the normal control group, the expression of Nrf2 gene and downstream antioxidant gene HO ⁃ 1 protein in the lung tissue of the ACR group increased, with the highest expression of chaperone protein Keap1 in the 10mg/(kg · d) group (P<0.01), The lowest expression was observed in the 10mg/(kg · d) group (P<0.01), while the expression of gene NQO ⁃ 1 protein gradually increased with the increase of ACR intake concentration (P<0.01)

　　Conclusion: Exposure to ACR in adolescent mice can lead to lung tissue damage, which may be related to oxidative reduction imbalance in lung tissue.