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. 2011 Sep;35(3):325-30.
doi: 10.5142/jgr.2011.35.3.325.

Red Ginseng Saponin Fraction a Isolated From Korean Red Ginseng by Ultrafiltration on the Porcine Coronary Artery

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Free PMC article

Red Ginseng Saponin Fraction a Isolated From Korean Red Ginseng by Ultrafiltration on the Porcine Coronary Artery

Young Hyun Jung et al. J Ginseng Res. .
Free PMC article

Abstract

Red ginseng saponin fraction-A (RGSF-A) contains a high percentage of panaxadiol saponins that were isolated from Korean red ginseng by ultrafiltration. The aim of this study was to elucidate the effects of RGSF-A on the porcine distal left anterior descending (LAD) coronary artery. The relaxant responses to RGSF-A were examined during contractions induced by 100 nM U46619 (9,11-dideoxy-9a,11a-methanoepoxy-prostaglandin F2a), a stable analogue of thromboxane A2. RGSF-A dose-dependently induced biphasic (fast- and slow-) relaxation in the distal LAD coronary artery in the presence of an intact endothelium. The fast-relaxation was quickly achieved in a minute, and then the slow-relaxation was slowly developed and sustained for more than thirty minutes after the administration of RGSF-A. The slow-relaxation had a tendency to be bigger than the fast-relaxation. Fast relaxation induced by RGSF-A was almost blocked by N ω-Nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor. However slow-relaxation induced by RGSF-A was only partially inhibited by L-NAME and ODQ. In the endothelium-removed ring, RGSF-A evoked only slow-relaxation to a certain extent. These data suggest that RGSF-A induced both endothelium dependent fast- and slow-relaxation and endothelium independent slow-relaxation in the porcine distal LAD coronary artery. The endothelium dependent fast-relaxation is mediated by the nitric oxide (NO)-cGMP pathway, and the endothelium dependent slow-relaxation is at least partially mediated by the NO-cGMP pathway. However, the endothelium-independent slow-relaxation remains to be elucidated.

Keywords: Endothelium; Ginseng; Nitric oxide; Porcine coronary artery; Red ginseng saponin fraction-A.

Figures

Fig. 1.
Fig. 1.. Red ginseng saponin fraction-A (RGSF-A) dose-dependently induced biphasic (fast- and slow-) relaxation in the distal left anterior descending coronary artery with the endothelium contracted by U46619. The fast-relaxation was quickly achieved in a minute, and then the slow-relaxation was slowly developed and sustained for more than thirty minutes after the administration of RGSF-A (A). The slow-relaxation had a tendency to be bigger than the fast-relaxation (B) (n=6).
Fig. 2.
Fig. 2.. Effects of red ginseng saponin fraction-A (RGSF-A) on the porcine coronary artery were inhibited by Nω-Nitro-L-arginine methyl ester (L-NAME). Administration of RGSF-A (100 μg/mL) induced fast- and slow- relaxation in the porcine distal left anterior descending coronary artery (A). Fast-relaxation by RGSF-A was almost abolished by L-NAME (100 μM) and slow- relaxation by RGSF-A was significantly attenuated by L-NAME (B,C). Both tracings were recorded from the same tissue (n=5, *p<0.05 vs. control).
Fig. 3.
Fig. 3.. Effects of red ginseng saponin fraction-A (RGSF-A) on the porcine coronary artery were inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin- 1-one (ODQ). Fast- and slow- relaxation were induced by RGSF-A in the distal left anterior descending coronary artery (A). Fast- relaxation evoked by RGSF-A was almost abolished by ODQ (10 μM) and the slow-relaxation was significantly attenuated by ODQ (B,C). Both tracings were recorded from the same tissue (n=5, *p<0.05).
Fig. 4.
Fig. 4.. Effects of red ginseng saponin fraction-A (RGSF-A) on the porcine distal left anterior descending (LAD) coronary artery without an endothelium. RGSF-A induced slow-relaxation to a small degree but did not evoke fast-relaxation in the distal LAD coronary artery without an endothelium.

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References

    1. Attele AS, Wu JA, Yuan CS. Ginseng pharmacology: multiple constituents and multiple actions. Biochem Pharmacol. 1999;58:1685–1693. doi: 10.1016/S0006-2952(99)00212-9. - DOI - PubMed
    1. Furukawa T, Bai CX, Kaihara A, Ozaki E, Kawano T, Nakaya Y, Awais M, Sato M, Umezawa Y, Kurokawa J. Ginsenoside Re, a main phytosterol of Panax ginseng, activates cardiac potassium channels via a nongenomic pathway of sex hormones. Mol Pharmacol. 2006;70:1916–1924. doi: 10.1124/mol.106.028134. - DOI - PubMed
    1. Cho JG, Lee MK, Lee JW, Park HJ, Lee DY, Lee YH, Yang DC, Baek N. Physicochemical characterization and NMR assignments of ginsenosides Rb1, Rb2, Rc, and Rd isolated from Panax ginseng. J Ginseng Res. 2010;34:113–121. doi: 10.5142/jgr.2010.34.2.113. - DOI
    1. Kaku T, Miyata T, Uruno T, Sako I, Kinoshita A. Chemico-pharmacological studies on saponins of Panax ginseng C. A. Meyer. II. Pharmacological part. Arzneimittelforschung. 1975;25:539–547. - PubMed
    1. Chang MS, Lee SG, Rho HM. Transcriptional activation of Cu/Zn superoxide dismutase and catalase genes by panaxadiol ginsenosides extracted from Panax ginseng. Phytother Res. 1999;13:641–644. doi: 10.1002/(SICI)1099-1573(199912)13:8<641::AID-PTR527>3.0.CO;2-Z. - DOI - PubMed

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