慢性心衰大鼠心肌细胞内三体蛋白和连接蛋白的表达变化  

Abnormal Intracellular Triandin and Junctin in Chronic Rat Heart Failure

作　　者：刘明明 牛治鑫 周永忠 胡淑婷 

机构地区：[1]宁夏医科大学基础医学院生理学系,银川750004

出　　处：《宁夏医科大学学报》2017年第11期1248-1251,共4页Journal of Ningxia Medical University

基　　金：国家自然科学基金(81260051;81760076)

摘　　要：目的观察慢性心衰大鼠心肌细胞三体蛋白和连接蛋白的表达变化,探讨三体蛋白和连接蛋白在大鼠慢性心衰中的机制。方法选取雄性SD大鼠30只,随机分为慢性心衰组和假手术组各15只。采用冠状动脉左前降支永久性结扎制作心梗模型。运用激光-扫描共聚焦显微镜以及蛋白免疫印迹等实验方法,检测28d后的心肌细胞肌浆网膜内钙离子的容量以及三体蛋白和连接蛋白的表达。结果慢性心衰组大鼠左室舒张末期压力(LVEDP)(8.61±2.14)mmHg低于假手术组(4.68±1.21)mmHg(P<0.01);慢性心衰组大鼠左室收缩期最大上升速率(dp/dtmax)(2350.18±172.44)mmHg·s^(-1)低于假手术组(4677.65±230.64)mmHg·s^(-1)(P<0.01);慢性心衰组大鼠钙瞬变峰值(ΔF/F0)(15.45±1.05)低于假手术组(54.72±2.12)(P<0.01)。慢性心衰组大鼠三体蛋白和连接蛋白的表达低于假手术组(P<0.01)。结论慢性心衰大鼠心肌细胞三体蛋白和连接蛋白表达降低、肌浆网对钙离子的固摄能力减弱。Objective To observe abnormal intracellular Triandin and Junctin in chronic rat heart failure（HF）.Methods Adult male SD rats were randomly received either myocardial infarction（MI）or a sham procedure.The myocardial infarction model was made by the permanent ligation of the left anterior descending coronary artery.The sarcoplasmic reticulum（SR）Ca^（2＋） content was investigated and the expression of Triandin and Junctin was assessed by using laser scanning confocal microscope and Western blot.Results There was a significant increase in the left ventricular end-diastolic pressure（LVEDP）in HF rats（8.61±2.14）mmHg compared with sham rats（4.68±1.21）mmHg（P〈0.01）.There was a significant decrease in the maximal change of systolic pressure over time（dp/dtmax）in HF rats（2350.18±172.44）mmHg·s^（-1） compared with control rats（4677.65±230.64）mmHg·s^（-1）（P〈0.01）.SR Ca^（2＋） content was dramatically reduced in HF myocytes（ΔF/F_0=15.45±1.05）compared with sham myocytes（ΔF/F_0=54.72 ±2.12）（P〈0.01）.The expression of Triandin and Junctin was significantly reduced in HF rat compared with sham group.Conclusion Down-regulation of Triandin and Junctin may be contribute to HF.

关 键 词：慢性心衰大鼠 肌浆网 三体蛋白 连接蛋白 

分 类 号：R541.6[医药卫生—心血管疾病]