利拉鲁肽激活Akt通路改善乳鼠心肌细胞缺氧/复氧损伤-东南大学学报医学版

利拉鲁肽激活Akt通路改善乳鼠心肌细胞缺氧/复氧损伤

单位：保定市第一中心医院内分泌二科, 河北保定 071000

分类号：R542.22;R33-33

出版年·卷·期（页码）：2017·36·第五期（764-768）

摘要：

目的：研究利拉鲁肽对乳鼠心肌细胞缺氧/复氧损伤的影响及机制。方法：分离乳鼠心肌细胞，分为对照组、缺氧/复氧组和利拉鲁肽组，体外构建缺氧/复氧损伤模型，使用流式细胞术检测细胞凋亡情况，Western blot检测凋亡相关蛋白caspase-3、Akt以及Akt磷酸化水平。结果：对乳鼠心肌细胞进行缺氧/复氧损伤处理后，流式细胞术检测发现，与对照组相比，缺氧/复氧损伤能明显诱导细胞凋亡，而利拉鲁肽则有抗凋亡作用；Western blot结果提示，缺氧/复氧损伤可诱导caspase-3表达，激活凋亡相关信号通路，促进细胞凋亡，而利拉鲁肽组细胞Akt磷酸化水平明显增加，caspase-3表达减少、活性降低。结论：利拉鲁肽可以通过增加Akt磷酸化以激活Akt通路，抑制caspase-3的表达，发挥抗凋亡作用，改善缺氧/复氧损伤。

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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