Objective:To study the effects of liraglutide on hypoxia/reoxygenation injury in neonatal rat cardiomyocytes and the underlying mechanism. Methods:The cardiomyocytes were isolated from neonatal rats, and then divided into control group, hypoxia/reoxygenation group and liraglutide group. The model of hypoxia/reoxygenation injury was established in vitro. Apoptosis was detected by flow cytometry and apoptosis related proteins including caspase-3, Akt, and phospho-Akt were detected by Western blot. Results:Cardiomyocytes of neonatal rats were treated with hypoxia/reoxygenation injury, compared with the control group, results of flow cytometry showed that hypoxia/reoxygenation injury could induce apoptosis of neonatal rat cardiomyocytes, while liraglutide had anti-apoptosis effects. Western blot showed that the expression of caspase-3 was activated by the hypoxia/reoxygenation injury. While in the liraglutide group, the phosphorylation of Akt was increased, as a result, the expression and activation of caspase-3 was suppressed. Conlusion:Liraglutide could improve the hypoxia/reoxygenation injury by increasing Akt phosphorylation to activate the Akt pathway, suppress the expression of caspase-3, and harbour an anti-apoptotic effect.
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