慢性心衰大鼠心肌细胞内异常的钙通道研究  

Abnormal intracellular calcium channel in rat with chronic heart failure

作　　者：宫京梅[1] 孙雪林 周永忠[3] 胡淑婷[4] 

机构地区：[1]宁夏医科大学第二附属医院心血管内科,宁夏银川750001 [2]宁夏中卫市人民医院妇产科,宁夏中卫755000 [3]宁夏医科大学基础医学院实验中心,宁夏银川750004 [4]宁夏医科大学基础医学院生理学系,宁夏银川750004

出　　处：《宁夏医学杂志》2014年第10期865-867,I0001,共4页Ningxia Medical Journal

基　　金：国家自然科学基金资助项目(81260051)

摘　　要：目的研究慢性心衰大鼠心肌细胞内异常的钙通道。方法将雄性SD大鼠被随机分为手术组和假手术组,运用激光扫描共聚焦显微镜、Western-blot等方法研究胞浆内咖啡因诱导钙瞬变及钙释放通道RyR2和其调节蛋白FKBP12.6表达的变化。结果慢性心衰大鼠心肌细胞内钙瞬变(ΔF/F0=11.9±0.9)显著低于对照组大鼠心肌细胞内钙瞬变(ΔF/F0=33.2±1.6,P<0.05);慢性心衰大鼠心肌细胞内FKBP12.6的表达较对照组下调。结论 FKBP12.6表达下调所致Ca2+泄漏是导致心衰的原因之一。Objective To study the abnormal intracellular calcium channel in rat with chronic heart failure （HF）. Methods Theadult male SD rats were randomized to receive either myocardial infarction （MI） or a sham procedure. The cytosolic caffe- ine -induced Ca2~ transients were investigated and the expression of ryanodine receptor （RyR2） and FKBP12.6 were assessed by using laser scanning confocal microscope and Western - blot. Results The cytosolic Ca2 ＋ transients were markedly reduced in amplitude in HF myocytes （ AF/F0 = 12.8 ＋ 1.2） compared with control myocytes （ AF/F0 = 32.8 ：t： I. 6, P 〈 0.05 ）, and the expression of FKBP 12.6 was significantly reduced in HF rat. Conclusion Diastolic sarcoplasmic reticulum Ca2 ＋ leak （ due to down - regulation of FKBP 12.6） mac contribute to HF.

关 键 词：心力衰竭 肌浆网 钙瞬变 雷尼丁受体 FK506结合蛋白 

分 类 号：R541.6[医药卫生—心血管疾病]