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国家卫生健康委员会
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英文作者:Kong Hongliang1 Zhao Yuting2 Jiang Yukun1 Tian Meijing2 Wang Huipan2 Ma Caobin1
单位:1辽宁省人民医院中国医科大学人民医院心脏中心,沈阳110013;2大连医科大学在读硕士研究生116044
英文单位:1Cardiology Center the People′s Hospital of Liaoning Province the People′s Hospital of China Medical University Shenyang 110013 China; 2Postgraduate of Dalian Medical University Dalian 116044 China
关键词:心力衰竭;人参皂苷Rb1;线粒体膜电位;电压依赖性阴离子通道
英文关键词:Heartfailure;Ginsenosides-Rb1;Mitochondrialmembranepotential;Voltagedependentanionchannel
目的 探讨人参皂苷Rb1(Gs-Rb1)对心力衰竭大鼠线粒体膜电位的影响。方法阿霉素诱导的心力衰竭大鼠随机分为心力衰竭组(16只)和Gs-Rb1组(18只),另外10只大鼠按阿霉素注射方法注射等量0.9%氯化钠注射液作为对照组。干预4周后,均完成心脏超声左心室射血分数(LVEF)检查。分别测定大鼠血清N末端B型脑钠肽前体(NT-proBNP)水平、线粒体膜电位和线粒体肿胀度,同步蛋白质印迹法检测线粒体钠钙交换体(NCLX)、线粒体钙离子单向转运体(MCU)、电压依赖性阴离子通道(VDAC)和线粒体钙离子摄入蛋白1(MICU1)等蛋白水平。结果 Gs-Rb1组LVEF高于心力衰竭组,而NT-proBNP水平低于心力衰竭组[(47±3)%比(37±5)%、(774±200)ng/L比(2 073±827)ng/L](均P<0.01)。Gs-Rb1组线粒体膜电位高于心力衰竭组,线粒体肿胀度小于心力衰竭组(均P<0.01)。Gs-Rb1组NCLX、VDAC、MICU1水平显著高于心力衰竭组,MCU水平低于心力衰竭组(均P<0.01)。结论 Gs-Rb1可能通过调节心肌细胞内线粒体膜电位改善心力衰竭,其可能通过NCLX等实现。
Objective To discuss the effect of ginsenoside Rbl(Gs-Rb1) on mitochondrial membrane potential in rats with heart failure(HF). Methods Adriamycin-induced rats with HF were randomly divided into HF group(16 rats) and Gs-Rb1 group(18 rats);0.9% sodium chloride injection group was as control(10 rats). After 4 weeks of intervention, the left ventricular ejection fraction(LVEF) was analyzed by echoeardiography. Serum lipid N-terminal B-type natriuretic peptide(NT-proBNP), mitochondrial membrane potential and mitochondrial swelling were anlyzed. Mitochondrial Na+/Ca2+ exchanger(NCLX), mitochondrial calcium uniporter(MCU), voltage dependent anion channel(VDAC) and mitochondrial calcium uptake 1(MICU1) were analyzed by western bolt. Results The LVEF in Gs-Rb1 group was higher than that in HF group, the NT-proBNP level was lower than that in HF group[(47±3)% vs (37±5)%,(774±200)ng/L vs (2 073±827)ng/L](both P<0.01). The mitochondrial membrane potential in Gs-Rb1 group was higher than that in HF group; the mitochondrial swelling was lower than that in HF group (both P<0.01). The levels of NCLX, VDAC and MICU1 in Gs-Rb1 group were significantly higher than those in HF group, and the level of MCU in Gs-Rb1 group was lower than that in HF group (all P<0.01). Conclusion Gs-Rb1 may improve HF by regulating mitochondrial membrane potential in cardiomyocytes, which may be related to NCLX.
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