人参皂苷Rb1对心力衰竭大鼠线粒体膜电位的影响

Effect of ginsenoside Rbl on mitochondrial membrane potential in rats with heart failure

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.