动物造模 z-bio 2022-09-21 339

　　Objective: To explore the expression changes and effects of BDNF, TrkB receptor and BDNF/TrkB signaling pathway in acute hypoxia and hypoxia preconditioning mice, to further improve the molecular mechanism of hypoxia preconditioning neuroprotection, and to provide evidence for hypoxia preconditioning. Provide a theoretical basis for clinical application.

　　Methods: ICR mice were used as the subjects to construct acute hypoxia and hypoxia preconditioning mouse models. After 0-4 days of model building, BDNF and TrkB receptors in the hippocampus of mice were detected by Western blot and real-time PCR technology. Changes in expression and BDNF/TrkB signaling pathway activity in early and late phases.

　　Results: The study found that with the increase of hypoxia times, the tolerance time increased significantly (P<0.05). Compared with the control group, the expressions of BDNF and full-length TrkB receptors in the acute hypoxia and hypoxia preconditioning groups increased. Compared with the control group, the expression of truncated TrkB receptor showed a downward trend, and its mRNA expression in the early and late stages of hypoxia preconditioning was significantly increased (P<0.05). Compared with the control group, the activity of BDNF/TrkB signaling pathway in the acute hypoxia group was inhibited, while the activity of BDNF/TrkB signaling pathway in the hypoxia preconditioning group tended to increase, and the difference was significant in the late phase (P<0.05).

　　Conclusion: Hypoxic preconditioning may increase the expression of BDNF and increase its binding to TrkB receptor, as well as down-regulate the expression of truncated TrkB receptor and reduce the formation of heterodimers, thereby co-activating the BDNF/TrkB signaling pathway, and ultimately affecting the BDNF/TrkB signaling pathway. Neuroprotection in mice.