动物造模 z-bio 2021-12-14 228

　　Purpose: To compare the changes of TLR4-NF-κB P65 signaling pathway after influenza virus infection in mice of different ages.

　　Method: Using immunohistochemistry and RT-PCR techniques to detect the protein and mRNA expression of TLR4 and NF-κB P65 in the lung tissues of mice of different ages, and compare the changes in signal pathways of different ages of mice infected with influenza virus.

　　Results: (1) TLR4 protein expression in lung tissue: TLR4 protein expression in the young model group was the strongest, compared with the normal group and the adult model group, the difference was significant (P<0.05). (2) NF-κB P65 protein expression in lung tissue: The expression of NF-κB P65 protein in the young model group was the strongest, and the expression gradually increased with time. The difference between each time point and the previous time point was significant (P<0.05). (3) TLR4 mRNA expression in lung tissue: The expression of TLR4 mRNA in the young model group was the strongest, which was significantly higher than that of the normal group and the adult model group, and the difference was significant (P<0.05). (4) NF-κB P65 mRNA expression in lung tissue: The expression of NF-κB P65 mRNA in the young model group was the strongest, and the expression gradually increased as the disease progressed; compared with the normal group and the adult model group, the difference was significant (P<0.05).

　　Conclusion: The excessive activation of TLR4-NF-κB P65 signaling pathway may be one of the mechanisms of severe lung immune pathological damage in young mice.