摘要
目的:观察人参皂苷单体Rb1对豚鼠缺血心室肌细胞动作电位(AP)和L-型钙离子通道的影响。方法:Langendorff离体心脏逆向灌流法分离豚鼠心室肌细胞,随机选取心室肌细胞分为正常对照组、缺血组及Rb1100、200和400μmol.L-13个剂量组。应用全细胞电流钳模式记录心室肌细胞动作电位,应用电压钳模式记录L-型钙离子通道电流(Ica-L)。结果:Rb1100、200和400μmol.L-1组缺血心室肌细胞动作电位复极50%(APD50)和动作电位复极90%(APD90)明显低于给药前(P<0.05或P<0.001),缺血后的心室肌细胞L-型钙离子通道峰值电流明显低于给药前(P<0.05或P<0.01)。Rb1抑制缺血心室肌细胞钙离子通道的开放,随浓度增加钙电流显著降低,具有浓度依赖性。结论:Rb1缩短缺血心肌细胞AP时程和抑制钙通道的作用,可能是其抗心肌缺血的机制之一。
Objective To investigate the effects of panaxadiol saponins monomer Rb1 on action potential （AP） and L-type calcium channel in ischemic cardiomyocytes of guinea pigs. Methods The Langendorff perfusion method was used to isolate the ventricular myocytes of guinea pigs and the ventricular myocytes were randomly divided into normal control group, ischemia group and three dose groups of Rb1 （100, 200 and 400 μm· L^- 1）. The AP of ventricular myocytes was recorded by current-clamp mode and the current of L-type calcium channel was recorded by voltage-clamp mode using whole clamp technique. Results Compared with ischemic cardiomyocytes group, the action potential duration （APD50） and （APD90） were decreased in 100, 200 and 400 /mμ· L^-1 Rb1 groups （P〈 0. 05 or P 〈0. 001）, the peak current of L-type calcium channel in ischemic cardiomyocytes was decreased singnificantly （P〈0.05 or P〈0.01） after Rb1 was administered. Panaxadiol saponins monomer Rb1 inhibited the opening of calcium channel in ischemic cardiomyocytes, the effect of calcium current was reduced with the increasing of Rb1 dose in a dose -dependent manner. Conclusion Panaxadiol saponins monomer Rb1 can shorten AP duration of ischemic cardiomyocytes and inhibit the opening of calcium channel which may be one of the critical mechanisms of anti-myocardial ischemia of panaxadiol saponins monomer Rb1.
出处
《吉林大学学报（医学版）》
CAS
CSCD
北大核心
2007年第6期978-981,共4页
Journal of Jilin University：Medicine Edition
基金
吉林省科技厅基金资助课题(吉科合字第19990302)
吉林省中医药管理局中医药科研课题(2004-081)
关键词
人参皂甙
心肌/细胞学
动作电位
钙通道
L型
panaxosides
myocardium/cytology
action potentials
calcium channels, L-type
