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Effects of Korean Red Ginseng Extract on Cisplatin-Induced Nausea and Vomiting
Kim Jong-Hoon,Yoon In-Soo,Lee Byung-Hwan,Choi Sun-Hye,Lee Jun-Ho,Lee Joon-Hee,Jeong Sang Min,Kim Seok-Chang,Park Chae-Kyu,Lee Sang-Mok,Nah Seung-Yeol The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.6
Ginseng, the root of Panax ginseng CA Meyer, is well known as a tonic medicine for restoring and enhancing human health. In traditional medicine, ginseng is utilized for the alleviation of emesis, which includes nausea and vomiting. However, it has not yet been demonstrated whether ginseng exhibits in vivo anti-nausea and anti-vomiting properties. In this study, we examined the anti-emetic effect of Korean red ginseng total extract (KRGE) on cisplatin-induced nausea and vomiting using ferrets. Intraperitoneal administration (i.p.) of cisplatin (7.5 mg/kg) induced both nausea and vomiting with one-hour latency. The episodes of nausea and vomiting reached a peak after 1.5 h and persisted for 3 h. Treatment with KRGE via oral route significantly reduced the cisplatin-induced nausea and vomiting in a dose-dependent manner. The anti-emetic effect was 12.7 $\pm$ 8.6, 31.8 $\pm$ 6.9, and 67.6 $\pm$ 4.0$\%$ with doses of 0.3, 1.0, and 3.0 g/kg of KRGE, respectively. Pretreatment with KRGE via oral route 1 and 2 h before cisplatin administration also significantly attenuated the cisplatin-induced nausea and vomiting. However this did not occur with a pretreatment 4 h before cisplatin administration. These results are supportive of KRGE being utilized as an anti-emetic agent against nausea and vomiting caused by chemotherapy (i.e. cisplatin).
Lee, Jun-Ho,Shin, Eun-Joo,Jeong, Sang Min,Kim, Jong-Hoon,Lee, Byung-Hwan,Yoon, In-Soo,Lee, Joon-Hee,Choi, Sun-Hye,Lee, Sang-Mok,Lee, Phil Ho,Kim, Hyoung-Chun,Nah, Seung-Yeol Elsevier 2006 european journal of pharmacology Vol.536 No.1
<P><B>Abstract</B></P><P>We previously demonstrated that dextromethorphan (DM; 3-methoxy-17-methylmorphinan) analogs have neuroprotective effects, and a recent report showed that DM reduces the adverse effects of morphine and blocks α<SUB>3</SUB>β<SUB>4</SUB> nicotinic acetylcholine receptors, a major target of anti-addictive agents. Here, we investigated the effects of DM, three of its analogs (DF, 3-methyl-17-methylmorphinan; AM, 3-allyloxy-17-methoxymorphian; and CM, 3-cyclopropyl-17-methoxymorphinan) and one of its metabolites (HM; 3-methoxymorphinan), on neuronal α<SUB>3</SUB>β<SUB>4</SUB> nicotinic acetylcholine receptor channel activity expressed in <I>Xenopus laevis</I> oocytes, using the two-microelectrode voltage clamp technique. We found that intraoocyte injection of neuronal α3 and β4 nicotinic acetylcholine receptor subunit cRNAs elicited an inward current (<I>I</I><SUB>ACh</SUB>) in the presence of acetylcholine. Co-treatment with DM, DF, AM, CM or HM inhibited <I>I</I><SUB>ACh</SUB> in a dose-dependent, voltage-independent and reversible manner. The IC<SUB>50</SUB> values for DM, DF, AM, CM and HM were 19.5±5.2, 15.8±4.5, 16.3±1.7, 10.1±2.8, and 13.5±4.0?μM, respectively. The order of potency for the inhibition of <I>I</I><SUB>ACh</SUB> was CM > HM > DF = AM > DM in oocytes expressing α3β4 nicotinic acetylcholine receptors. The inhibitions of (<I>I</I><SUB>ACh</SUB>) by DM, DF and HM, AM and CM were non-competitive. These results indicate that AM, CM and HM could be novel non-competitive agents regulating α<SUB>3</SUB>β<SUB>4</SUB> nicotinic acetylcholine receptor channel activity.</P>
Effects of Ginsenosides and Their Metabolites on Voltage-dependent Ca2+ Channel Subtypes
Jun-Ho Lee,Sang Min Jeong,Jong-Hoon Kim,Byung-Hwan Lee,In-Soo Yoon,Joon-Hee Lee,Sun-Hye Choi,Sang-Mok Lee,Yong-Sun Park,이정하,Sung Soo Kim,Hyoung-Chun Kim,Boo-Yong Lee,Seung-Yeol Nah 한국분자세포생물학회 2006 Molecules and cells Vol.21 No.1
In previous reports we demonstrated that ginsenosides, active ingredients of Panax ginseng, affect some subsets of voltage-dependent Ca2+ channels in neuronal cells expressed in Xenopus laevis oocytes. However, the major component(s) of ginseng that affect cloned Ca2+ channel subtypes such as α1C (L)-, α1B (N)-, α1A (P/Q)-, α1E (R)- and α1G (T) have not been identified. Here, we used the two-microelectrode voltage clamp technique to characterize the effects of ginsenosides and ginsenoside metabolites on Ba2+ currents (IBa) in Xenopus oocytes expressing five different Ca2+ channel subtypes. Exposure to ginseng total saponins (GTS) induced voltage-dependent, dose-dependent and reversible inhibition of the five channel subtypes, with particularly strong inhibition of the α1G-type. Of the various ginsenosides, Rb1, Rc, Re, Rf, Rg1, Rg3, and Rh2, ginsenoside Rg3 also inhibited all five channel subtypes and ginsenoside Rh2 had most effect on the α1C- and α1E-type Ca2+ channels. Compound K (CK), a protopanaxadiol ginsenoside metabolite, strongly inhibited only the α1G-type of Ca2+ channel, whereas M4, a protopanaxatriol ginsenoside metabolite, had almost no effect on any of the channels. Rg3, Rh2, and CK shifted the steady-state activation curves but not the inactivation curves in the depolarizing direction in the α1B- and α1A-types. These results reveal that Rg3, Rh2 and CK are the major inhibitors of Ca2+ channels in Panax ginseng, and that they show some Ca2+ channel selectivity.