利拉鲁肽激活Akt通路改善乳鼠心肌细胞缺氧/复氧损伤  

Liraglutide activates the Akt pathway to improve myocardial cells of neonatal rats with hypoxia/reoxygenation injury

作　　者：张文娟[1] 周雪[1] 李瑞雪[1] 杨茜[1] 夏丽芳[1] 李志红[1] 

机构地区：[1]保定市第一中心医院内分泌二科,河北保定071000

出　　处：《东南大学学报（医学版）》2017年第5期764-768,共5页Journal of Southeast University(Medical Science Edition)

基　　金：保定市科学技术研究与发展指导计划项目(16ZF110)

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 antiapoptosis 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.

关 键 词：利拉鲁肽 缺氧/复氧损伤 AKT通路 细胞凋亡 乳鼠 

分 类 号：R542.22[医药卫生—心血管疾病] R33-33[医药卫生—内科学]