中文摘要：

Liraglutide 是为与类型 2 糖尿病 mellitus 对待病人的象 glucagon 一样 peptide-1 受体收缩筋。我们的以前的研究证明了 liraglutide 通过与经历经皮的冠的干预的尖锐心肌的梗塞在病人改进 endothelial 功能保护心脏的功能。现在的学习将调查 liraglutide 是否能对灌注 injury.MethodsIn vitro 实验在 cardiomyocytes 上执行直接保护的效果用 H9C2 房间和新生的老鼠被执行经历模拟 hypoxia/reoxygenation (H/R ) 的室的 cadiomyocytes 感应。Cardiomyocytes apoptosis 被荧光 TUNEL 检测。Mitochondrial 膜潜力(m) 和细胞内部的反应的氧种类(ROS ) 被 JC-1 和 DHE 分别地估计。Fura-2/AM 被用来测量细胞内部的 Ca ²⁺ 集中和钙短暂。染色的 Immunofluorescence 被用来估计 sarcoplasmic 蜂窝胃 Ca ²⁺-ATPase (SERCA2a ) 的表示水平。在 vivo 实验， SERCA2a 的心肌的 apoptosis 和表示被比色的 TUNEL 并且由染色的 immunofluorescence 检测， respectively.ResultsIn vitro liraglutide 对 H/R 禁止了 cardiomyotes apoptosis。cardiomyocytes 的 m 比 H/R 组在 liraglutide 组是更高的。H/R 在被 liraglutide 稀释的 H9C2 房间增加了 ROS 生产。Liraglutide 显著地降低了超载和与 H/R 相比短暂的改进的钙组织的 Ca ²⁺ 。染色结果的 Immunofluorescence 证明 liraglutide 支持了在 H/R 组被减少的 SERCA2a 表示。在 ischemia/reperfusion 老鼠心， apoptosis 显著地被稀释， SERCA2a 表示被 liraglutide 与 H/R group.ConclusionsLiraglutide 相比增加能直接通过细胞内部的钙动态平衡的调整可能保护 cardiomyocytes 免于是的灌注损害。

英文摘要：

Background Liraglutide is glucagon-like peptide-1 receptor agonist for treating patients with type 2 diabetes mellitus. Our previous studies have demonstrated that liraglutide protects cardiac function through improving endothelial function in patients with acute myocardial infarction undergoing percutaneous coronary intervention. The present study will investigate whether liraglntide can perform direct protective effects on cardiomyocytes against reperfusion injury. Methods In vitro experiments were performed using H9C2 cells and neonatal rat ventricular cadiomyocytes undergoing simulative hypoxia/reoxygenation （H/R） induction. Cardiomyocytes apoptosis was detected by fluorescence TUNEL. Mitochondrial membrane potential （AWm） and intracellular reactive oxygen species （ROS） was assessed by JC-1 and DHE, respectively. Fura-2/AM was used to measure intracellular Ca2＋ concentration and calcium transient. Immtmofluorescence staining was used to assess the expression level of sarcoplasmic reticulum Ca2＋-ATPase （SERCA2a）. In vivo experiments, myocardial apoptosis and expression of SERCA2a were detected by colorimetric TUNEL and by immunofluorescence staining, respectively. Results In vitro liraglutide inhibited cardiomyotes apoptosis against H/R. △mψ of cardiomyocytes was higher in liraglntide group than H/R group. H/R increased ROS production in H9C2 cells which was attenuated by liraglutide. Liraglutide significantly lowered Ca2＋ overload and improved calcium transient compared with H/R group, lmmunofluorescence staining results showed liraglutide promoted SERCA2a expression which was decreased in H/R group. In ischemia/reperfusion rat hearts, apoptosis was significantly attenuated and SERCA2a expression was increased by liraglutide compared with H/R group. Conclusions Liraglutide can directly protect cardiomyocytes against reperfusion injury which is possibly through modulation of intracellular calcium homeostasis.