Maslov L N, Konkovskaia Iu N
Eksp Klin Farmakol. 2009 Jul-Aug;72(4):52-60.
The review systematizes data on the cardiotropic effects of ginsenosides studied in vivo and in vitro. It has been shown that ginsenosides decrease the heart rate both in vivo and in vitro. It is established that triterpenoid saponins inhibit contractility of isolated heart and atrium and exhibit negative inotropic effect in the experiments with isolated cardiomyocytes. Ginsenosides shorten duration of the action potential and decrease the amplitude of slow action potential in cardiac cells. There is evidence that ginsenosides inhibit Ca2+ channels. Triterpenoid saponins of ginseng improve the cardiac tolerance to ischemic and reperfusive damage both in vivo and in vitro. These saponins increase cardiac resistance to the toxic action of isoproterenol and adriamycin. Triterpenoid saponins enhance the tolerance of cardiomyocytes to oxidative stress in vitro. Ginsenosides prevent the appearance of ischemic/reperfusive arrhythmias and decrease the incidence of arrhythmias induced by epinephrine. The molecular mechanisms of action of triterpenoid saponins is discussed and their interactions with steroidal hormone receptors, protein kinases, NO synthase, K(ATP) channels, and Ca2+ channels are considered.
该综述对人参皂苷在体内和体外研究的心脏效应数据进行了系统化整理。研究表明，人参皂苷在体内和体外均能降低心率。已证实三萜皂苷在离体心脏和心房实验中抑制收缩力，并在离体心肌细胞实验中表现出负性肌力作用。人参皂苷可缩短心脏细胞动作电位的持续时间，并降低慢动作电位的幅度。有证据表明人参皂苷可抑制钙离子通道。人参的三萜皂苷在体内和体外均能提高心脏对缺血和再灌注损伤的耐受性。这些皂苷可增强心脏对异丙肾上腺素和阿霉素毒性作用的抵抗力。三萜皂苷在体外可增强心肌细胞对氧化应激的耐受性。人参皂苷可预防缺血/再灌注心律失常的出现，并降低肾上腺素诱导的心律失常的发生率。文中讨论了三萜皂苷的分子作用机制，并考虑了它们与甾体激素受体、蛋白激酶、一氧化氮合酶、ATP敏感性钾通道和钙离子通道的相互作用。
