摘要
目的研究慢性心衰大鼠心肌细胞肌浆网雷尼丁受体及其调节蛋白FK506结合蛋白(Calstabin2)的异常表达。方法雄性SD大鼠25只,按照3∶2的比例随机分为心衰组(15只)和假手术组(10只),运用激光扫描共聚焦显微镜、Western-blot等方法研究2组大鼠心肌细胞肌浆网内钙容量及钙释放通道雷尼丁受体(Ry R2)和其调节蛋白Calstabin2表达的变化。结果慢性心衰大鼠心功能LVEDP(8.91±2.16)mm Hg、dp/dtmax(2 250.19±172.44)mm Hg/s,显著低于假手术组大鼠心功能LVEDP(4.17±1.15)mm Hg、dp/dtmax(4 822.54±221.62)mm Hg/s(P<0.05);慢性心衰大鼠心肌细胞肌浆网内钙容量ΔF/F0=25.3±2.8,显著低于假手术组大鼠肌浆网内钙容量ΔF/F0=47.8±3.5(P<0.05);慢性心衰大鼠心肌细胞内Calstabin2的表达较对照组下调。结论 Calstabin2的表达下调所致Ry R2稳定性下降是导致心衰的原因之一。
Objective To study abnormal intracellular ryanodine receptor and its regulatory protein Calstabin2 in chronic rat heart failure （HF）. Methods Adult male SD rats were randomized to divided into myocardial infarction （MI） group and sham operation group. We investigated the sarcoplasmic reticulum （SR） Ca2 ~ content and assessed the expression of ryanodine receptor （RyR2） and Calstabin2 by using laser scanning confocal microscope and Western - blot. Results There was a significant increase in the left ventrieu- lar end -diastolic pressure （LVEDP） in HF rats （8.91±2.16 mmHg,n = 15） compared with sham rats 44.17 ± 1.15 mmHg,n = 10, P 〈 O. 05）. There was a significant decrease in the maximal change of systolic pressure over time （dp/dtmax） in HF rats （2 250.19 ± 172.44 mmHg/s,n = 12） compared with control rats （4 822.54 ±221.62 mmHg/s,n = 10,P 〈0.05）. SR Ca^2＋ content was dramatic- ally reduced in HF myocytes （ AF/F0 = 25.3 ± 2.8, n = 12） compared with sham myocytes （ AF/F0 = 47.8 ± 3.5, n = 12,P 〈 O. 05 ）. The expression of Calstabin2 was significantly reduced in HF rat compared with sham group. Conclusion Stability decrease of RyR2 that due to down - regulation of Calstabin2 could contribute to HF.
出处
《宁夏医学杂志》
CAS
2017年第10期865-867,共3页
Ningxia Medical Journal
基金
宁夏自然科学基金资助项目(NZ15082)
