| Abstrakt: |
Objective: The aim of the current study was to observe the protective effect of GLP-1R agonist on hypoxia reoxygenation cardiomyocytes and to explore the role of GLP-1R/PI3K/AKT signaling pathway. Methods: H9c2 myocardial cells were randomly divided into four groups: control group, hypoxia reoxygenation model group (H/R), Exenatide group and PI3K/AKT signaling pathway inhibitor group. CCK-8 method was used to detectmyocardial enzymes, and the expression of Caspase-3, Bcl-2 and Bax proteins was detected byWestern blot. Results: The apoptosis rate in exenatide groupwas decreased than the H/R group. The levels of LDH and CK-MB in H/R group were higher than control group, which compared with the H/R group, exenatide group were decreased, and it in PI3K/AKT pathway inhibitor group were increased than exenatide group. The expression of Caspase-3 and Bax in H/R group was higher than that in control group group, and the level of Bcl-2 was decreased. Compared with H/R group, the levels of Caspase-3 and Bax in exenatide groupwere decreased, and the level of Bcl-2was increased. Compared with exenatide group, the levels of Caspase-3 and Bax were significantly increased in the PI3K/AKT pathway inhibitor group, and the level of Bcl-2 was decreased. Conclusion: Exenatide has protective effects on the cardiomyocytes during hypoxia reoxygenation injury. The GLP-1R/PI3K/AKT signaling pathway may be involved in the process that exenatide inhibiting cardiomyocyte apoptosis. [ABSTRACT FROM AUTHOR] |
