Kim N D, Kang S Y, Park J H, Schini-Kerth V B
Laboratory of Pharmacology, College of Pharmacy, Seoul National University, South Korea.
Eur J Pharmacol. 1999 Feb 12;367(1):41-9. doi: 10.1016/s0014-2999(98)00898-x.
The aim of the present study was to characterize the endothelium-dependent relaxation elicited by ginsenosides, a mixture of saponin extracted from Panax ginseng, in isolated rat aorta. Relaxations elicited by ginsenosides were mimicked by ginsenoside Rg1 and ginsenoside Rg1, two major ginsenosides of the protopanaxatriol group. Ginsenoside Rg3 was about 100-fold more potent than ginsenoside Rg1. The endothelium-dependent relaxation in response to ginsenoside Rg3 was associated with the formation of cycle GMP. These effects were abolished by N(G)-nitro-L-arginine and methylene blue. Relaxations in response to ginsenoside Rg3 were unaffected by atropine, diphenhydramine, [D-Pro2, D-Trp7,9]substance P, propranolol, nifedipine, verapamil and glibenclamide but were markedly reduced by tetraethylammonium. Tetraethylammonium modestly reduced the relaxation induced by sodium nitroprusside. These findings indicate that ginsenoside Rg3 is a major mediator of the endothelium-dependent nitric oxide-mediated relaxation in response to ginsenosides in isolated rat aorta, possibly via activation of tetraethylammonium-sensitive K+ channels.
本研究的目的是在离体大鼠主动脉中，对人参皂苷（从人参中提取的一种皂苷混合物）所引发的内皮依赖性舒张进行特性分析。原人参三醇组的两种主要人参皂苷——人参皂苷Rg1和人参皂苷Rg1模拟了人参皂苷所引发的舒张作用。人参皂苷Rg3的效力比人参皂苷Rg1强约100倍。人参皂苷Rg3所引发的内皮依赖性舒张与环鸟苷酸的形成有关。这些效应被N(G)-硝基-L-精氨酸和亚甲蓝消除。人参皂苷Rg3所引发的舒张不受阿托品、苯海拉明、[D-脯氨酸2，D-色氨酸7,9]P物质、普萘洛尔、硝苯地平、维拉帕米和格列本脲的影响，但被四乙铵显著降低。四乙铵适度降低了硝普钠所引发的舒张。这些发现表明，人参皂苷Rg3可能是通过激活对四乙铵敏感的钾通道，在离体大鼠主动脉中作为内皮依赖性一氧化氮介导的舒张反应的主要介质，该舒张反应是对人参皂苷而言的。
