The Relaxant Effect of Ginseng Saponin on the Bladder and Prostatic Urethra: An in vitro and in vivo Study

Abstract

Aim: To assess the effects of ginseng saponin on relaxation of the bladder and prostatic urethra and to determine its mechanism of action. Materials and Methods: For the in vitro study, prostatic urethra muscle strips were harvested from 18 male New Zealand rabbits. The strips were mounted in organ baths and connected to force displacement transducers. After stabilization, maximal tissue contractions were obtained by the application of phenylepinephrine to the urethra strips, and a dose-response curve for ginseng saponin was constructed (10^–6–10^–2M). After pretreatment of urethra strips with N-nitro-L-arginine methyl ester (L-NAME), another dose-response curve for ginseng saponin was constructed. For the in vivo study, we used adult male Sprague-Dawley rats divided into three groups [control, partial bladder outlet obstruction (PBOO) and saponin-fed groups], and we monitored the vesical pressure (P_ves) and urethral perfusion pressure (UPP). Results: The ginseng saponin induced a significant dose-dependent relaxant effect on the prostatic urethra strips. A significant relaxant effect of ginseng saponin was observed from 10^–3M, and ginseng saponin significantly relaxed urethra strips by 50.2 ± 20.26% at 10^–2M. The relaxant effect was partially inhibited with L-NAME pretreatment. In the in vivo study, the change in UPP between baseline and relaxation was significantly higher in the saponin group than in the control or PBOO group (p < 0.001). The saponin group showed a significantly lower baseline P_ves than the PBOO group. Conclusions: We observed a significant relaxation effect of ginseng saponin on the bladder and prostatic urethra in both in vitro and in vivo studies. The mechanism by which ginseng saponin induces relaxation appears to involve the nitric oxide/nitric oxide synthase pathway.

Anti-hypertensive Herbs and their Mechanisms of Action: Part I

“…The primary mechanism associated with ginseng -induced hypotensive effect is attributed to an improvement in arterial function. Indeed, ginseng causes a dramatic increase in eNOS expression and NO production (Valli and Giardina, 2002 ; Jang et al, 2011 , 2012 ; Hong et al, 2012 ; Pan et al, 2012 ; Table 2 ). Ginsenoside Rg3 (red ginseng ) is known to activate eNOS (Valli and Giardina, 2002 ; Jang et al, 2011 ), increase NO and cGMP levels, as well as activate Ca 2+ -gated potassium channels (Kim et al, 1999b ).…”

Conversion of Ginsenoside Rb1 into Six Types of Highly Bioactive Ginsenoside Rg3 and Its Derivatives by FeCl₃ Catalysis

“…5) Ginsenoside Rb1 cannot be directly absorbed by the human body due to the four glycosides of 3-O-Glc-Glc-and 20-O-Glc-Glc-substituted on the Rb1 molecular core, so Rb1 has low bioavailability. [6][7][8] After oral intake of ginseng, the major natural ginsenosides are hydrolyzed in the human intestinal tract, and the major ginsenosides are converted into more active forms of the minor ginsenosides, which are subsequently absorbed and can then exhibit their physiological activity; however, the rates of conversion are very low. [9][10][11][12] The minor ginsenosides Rg3, Rg5, Rk1 and other derivatives have various important pharmacological activities such as antitumor, antidiabetes, antithrombotic and anti-Alzheimer's disease effects.…”