【摘要】 目的:探讨参三七皂苷Rb1预处理对肥厚心肌细胞缺氧/复氧(H/R)损伤游离钙([Ca2+]i)的影响及其与心肌细胞保护作用与关系。方法:采用体外培养乳鼠心肌细胞,血管紧张素I(IAngII)刺激形成肥厚模型,实验分为7组:①正常对照组(C);②肥厚细胞模型对照组;③肥厚细胞H/R损伤组(H+H/R);④-⑦:Rb1预处理(0.01～10μmol/L)+H/R组;用激光共聚焦显微镜测定[Ca2+]i以及对电压依赖和受体操纵性激动剂KCl,NE诱发细胞内钙离子变化的影响。结果:经缺氧2h复氧1h后,肥厚细胞H/R组[Ca2+]i荧光强度较对照组显著增高,Rb1预处理组细胞内[Ca2+]i荧光强度较肥厚细胞H/R损伤组显著降低(P<0.01)。Rb1预处理使KCl、NE诱发的细胞内钙荧光强度仅增加61.3%和78.9%,升幅显著下降(P<0.01)。结论:参三七皂苷Rb1预处理具有显著减轻H/R肥厚心肌细胞钙超载作用,是其细胞保护作用的重要机制。更多还原

【Abstract】 Objective:To explore the role of pretreatment of panax notoginsenoside Rb1 on free calcium( i) in protecting effective against hypoxia/reoxygenation(H/R)injury against in neonatal rat hypertrophied cardiomyocytes.Methods: The primary culture of neonatal rat cardiomyocytes was stimulated by angiotensin II(AngII) and H/R model was undergone with 2h of hypoxia followed by 1h reoxygenation.The cardiomyocytes were divided into 7 groups:①normal control group;②AngII hypertrophy model control group;③hypertrophied cardiomyocytes +H / R group;④～⑦: Rb1 pretreatment(0.01-10 μmol/L) +H/R group under voltage-dependent or receptor agonists scanning confocal microscopy in which the i fluorescence intensity were determined and effecting on KCl,NE induced change of i concentration were observed.Results: After hypoxia 2h reoxygenation followed by 1h,the i fluorescence intensity of control group immediately began to increase,the i fluorescence intensity of H/R group was significantly higher(P<0.01).Pretreatment with Rb1 for 48h,the i fluorescence intensity was significantly lower than that of H/R group.Rb10.01-10μmol/L pretrement could decrease KCl,NE-induced increasing ofi fluorescence intensity significantly,which increased by only 61.3 and 78.9%(P<0.01).Conclusion: These suggested that mechanistic of protective effect of Panax notoginseng saponins Rb1 against H/R injury may be associated with their reducing intracellular calcium overload and maintenance of calcium homeostasis of hypertrophied cardiomyocytes.更多还原