Research 3
Studies on Organic Germanium
 Studies on Rb1, Rb2 Studies on Rc, Rd, Re
Studies on Rg1, Rg2 and Rg3
 Studies on Rh1, Rh2
 Studies on Wild American Ginseng
           
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Related Research -- Studies on Rc, Rd, Re

More studies on Rc (> 97 articles):

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Rc%20ginseng

More studies on Rd (> 105 articles):

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Rd%20ginseng

More studies on Re (> 153 articles):

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Re%20ginseng

Study One
American ginseng berry extract and ginsenoside Re attenuate cisplatin-induced kaolin intake in rats.
Mehendale S, Aung H, Wang A, et al., Cancer Chemother Pharmacol. 2005 Jul; 56(1):63-9. Epub 2005 Mar 25
Tang Center for Herbal Medicine Research, The Pritzker School of Medicine, University of Chicago, IL 60637, USA.
PURPOSE: Cisplatin, a chemotherapeutic agent, causes significant nausea and vomiting. It is postulated that cisplatin-induced oxidant stress may be responsible for these symptoms. We tested whether pretreatment with American ginseng berry extract (AGBE), an herb with potent antioxidant capacity, and one of its active antioxidant constituents, ginsenoside Re, could counter cisplatin-induced emesis using a rat pica model. METHODS: In rats, exposure to emetic stimuli such as cisplatin causes significant kaolin intake, a phenomenon called pica. We therefore measured cisplatin-induced kaolin intake as an indicator of the emetic response. Rats were pretreated with vehicle, AGBE (dose range 50-150 mg/kg, IP) or ginsenoside Re (2 and 5 mg/kg, IP). Rats were treated with cisplatin (3 mg/kg, IP) 30 min later. Kaolin intake, food intake, and body weight were measured every 24 h for 120 h. Additionally, the free radical scavenging activity of AGBE was measured in vitro using ESR spectroscopy. RESULTS: A significant dose-response relationship was observed between increasing doses of pretreatment with AGBE and reduction in cisplatin-induced pica. Kaolin intake was maximally attenuated by AGBE at a dose of 100 mg/kg. Food intake also improved significantly at this dose (P<0.05). Pretreatment with ginsenoside Re (5 mg/kg) also decreased kaolin intake (P<0.05). In vitro studies demonstrated a concentration-response relationship between AGBE and its ability to scavenge superoxide and hydroxyl radicals. CONCLUSION: Pretreatment with AGBE and its major constituent, Re, attenuated cisplatin-induced pica, and demonstrated potential for the treatment of chemotherapy-induced nausea and vomiting. Significant recovery of food intake further strengthens the conclusion that AGBE may exert an antinausea/antiemetic effect.

Study Two
Effects of selected ginsenosides on phorbol ester-induced expression of cyclooxygenase-2 and activation of NF-kappaB and ERK1/2 in mouse skin
Surh YJ, Lee JY, Choi KJ, Ko SR, Ann N Y Acad Sci. 2002 Nov;973:396-401
Our previous studies have demonstrated that the methanol extract of heat-processed Panax ginseng C.A. Meyer exerts antioxidative, antiinflammatory, and anti-tumor-promoting effects. In the present study, we examined the antiinflammatory effects of several ginsenosides (Rb(1), Rc, Re, Rg(1), Rg(3)) derived from P. ginseng. Topical application of each of these ginsenosides significantly attenuated ear edema induced by 12-O-tetradecanoylphorbol-13-acetate (TPA). These ginsenosides also suppressed expression of cyclooxygenase-2 (COX-2) and activation of NF-kappaB in the TPA-treated dorsal skin of mice. Of the ginsenosides tested, Rg(3) was found to be most effective in terms of inhibiting TPA-induced ear edema, COX-2 expression, and NF-kappaB activation.

Study Three

Ginseng extract inhibits lipolysis in rat adipocytes in vitro by activating phosphodiesterase 4.
Wang H, Reaves LA, Edens NK, Journal of Nutrition. 2006 Feb;136(2):337-42
The Ohio State University, Columbus, OH 43210, USA.

Ginseng extract inhibits lipolysis in rat adipocytes in vitro by activating phosphodiesterase 4.

Wang H, Reaves LA, Edens NK, Journal of Nutrition. 2006 Feb;136(2):337-42

The Ohio State University, Columbus, OH 43210, USA.

Elevated concentrations of plasma free fatty acids (FFA) may cause insulin resistance. Inhibition of lipolysis reduces FFA availability and improves insulin sensitivity. Ginseng extract (Panax spp., GE) was shown to improve glycemia in Type 2 diabetes. In the present study, the antilipolytic effect of GE in rat adipocytes and the signaling pathway for GE antilipolysis were investigated. Adipocytes were isolated from rat fat tissue by collagenase digestion. The ability of GE to inhibit lipolysis was assessed by measuring glycerol and FFA release into the incubation medium. Phosphatidylinositol 3-kinase (PI3-K) inhibitor and various phosphodiesterase (PDE) inhibitors were applied to investigate the signaling pathway for GE antilipolysis. The present study showed that insulin and GE inhibited lipolysis by 42.4 and 49% compared with basal, respectively (P < 0.05). Unlike insulin, the PI3-K inhibitor wortmannin did not reverse GE antilipolysis, and GE did not affect phosphorylation of protein kinase B (PKB). The nonselective PDE inhibitor enprofylline reversed both insulin and GE antilipolysis. The specific phosphodiesterase 3 (PDE3) inhibitor cilostamide reversed insulin antilipolysis completely, but did not significantly affect GE antilipolysis. The specific phosphodiesterase 4 (PDE4) inhibitor rolipram did not significantly affect insulin antilipolysis, but almost completely reversed GE antilipolysis. Moreover, the combination of PDE3 and PDE4 inhibitors completely reversed GE antilipolysis. None of the ginsenosides (Rb1, Re, Rg1, Rc, Rb2, and Rd) were responsible for GE antilipolysis. The results suggest that ginseng exerts its antilipolytic effect through a signaling pathway different from that of insulin. GE antilipolysis is mediated in part by activating PDE4 in rat adipocytes
Study Four
Antioxidant effects of ginsenoside Re in cardiomyocytes
Xie JT, Shao ZH, Vanden Hoek TL, et al., Eur J Pharmacol. 2006 Feb 27; 532(3):201-7. Epub 2006 Feb 21
Tang Center for Herbal Medicine Research, School of Medicine, University of Chicago; Department of Anesthesia and Critical Care, School of Medicine, University of Chicago, Chicago, IL 60637, USA
We have previously demonstrated that American ginseng berry extract exhibited significant protection against oxidant-mediated injury in cardiomyocytes. To extend this work, we sought to investigate the antioxidant effects of Re, a protopanaxatriols-type and single chemical integrant present in American ginseng berry extract, using the same chick cardiomyocyte model of oxidant injury as well as ESR spectroscopy in a cell-free chemical system. In cells exposed to 2 h of H(2)O(2) (0.5 mM), pretreatment with Re (0.05, 0.1, or 0.5 mg/ml for 2 h) significantly attenuated 2',7'-dichlorofluorescein (DCF) fluorescence by 51% (from 1345+/-67 to 658+/-46 a.u., P<0.001), and remarkably reduced cell death (from 51.5+/-3.0% to 11.8+/-1.5%, P<0.001, compared to the control). Similar results were also observed in cells exposed to antimycin A (100 muM), a mitochondrial electron transport chain site III inhibitor which increases endogenous oxidative stress. In the ESR study, however, Re failed to reduce the formation of the superoxide/DMPO adduct and DPPH radicals. These results suggest that ginsenoside Re functions as an antioxidant, protecting cardiomyocytes from oxidant injury induced by both exogenous and endogenous oxidants, and that its protective effects may be mostly attributed to scavenging H(2)O(2) and hydroxyl radicals

Study Five
Metabolism of ginsenoside Re by human intestinal microflora and its estrogenic effect
Bae EA, Shin JE, Kim DH, Biol Pharm Bull. 2005 Oct;28(10):1903-8
College of Pharmacy, Kyung Hee University; Seoul, 130-701 Korea

Metabolism of ginsenoside Re by human intestinal microflora and its estrogenic effect

Bae EA, Shin JE, Kim DH, Biol Pharm Bull. 2005 Oct;28(10):1903-8

College of Pharmacy, Kyung Hee University; Seoul, 130-701 Korea

To understand the relationship between the metabolism and biological activity of ginsenoside Re, a main protopanaxatriol saponin in Panax ginseng C. A. MEYER, its metabolic pathway and estrogenic effect by human intestinal microflora were investigated. All human fecal specimens metabolized ginsenoside Re, mainly to ginsenoside Rh1 and ginsenoside F1, via ginsenoside Rg1, with protopanaxadiol as a minor component. Almost all isolated ginsenoside Re-metabolizing intestinal bacteria (GHIB) also metabolized ginsenoside Re, mainly to ginsenosides Rh1 and F1, via ginsenoside Rg1. Alpha-Rhamnosidase and beta-glucosidase, partially purified from the most potent GHIB, Bacteroides JY-6, hydrolyzed ginsenoside Re and ginsenoside Rg1, respectively; however, they did not hydrolyze ginsenosides Rh1 and F1. These findings suggest that the ginsenosides Rh1 and/or F1 may not be suitable substrates of intestinal bacteria, particularly Bacteroides JY-6. The estrogenic effects of ginsenoside Re and its main metabolites, ginsenosides Rg1 and Rh1, were also investigated. Ginsenoside Rh1 showed the greatest estrogenic effect in human breast carcinoma MCF-7 cells. Based on these findings, the estrogenic effect of ginsenoside Re may be expressed by intestinal microflora

Study Six
A natural compound (ginsenoside Re) isolated from Panax ginseng as a novel angiogenic agent for tissue regeneration.
Huang YC, Chen CT, Chen SC, et al., Pharm Res. 2005 Apr;22(4):636-46. Epub 2005 Apr 7

PURPOSE: The primary challenge for tissue engineering is to develop a vascular supply that can support the metabolic needs of the engineered tissues in an extracellular matrix. In this study, the feasibility of using a natural compound, ginsenoside Re, isolated from Panax ginseng in stimulating angiogenesis and for tissue regeneration was evaluated. METHODS: Effects of ginsenoside Re on the proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs) were examined in vitro. Additionally, angiogenesis and tissue regeneration in a genipin-fixed porous acellular bovine pericardium (extracellular matrix; ECM) incorporated with ginsenoside Re implanted subcutaneously in a rat model were investigated. Basic fibroblast growth factor (bFGF) was used as a control. RESULTS: It was found that HUVEC proliferation, migration in a Transwell plate, and tube formation on Matrigel were all significantly enhanced in the presence of bFGF or ginsenoside Re. Additionally, effects of ginsenoside Re on HUVEC proliferation, migration, and tube formation were dose-dependent and reached a maximal level at a concentration of about 30 microg/ml. The in vivo results obtained at 1 week postoperatively showed that the density of neocapillaries and the tissue hemoglobin content in the ECMs were significantly enhanced by bFGF or ginsenoside Re. These results indicated that angiogenesis in the ECMs was significantly enhanced by loading with bFGF or ginsenoside Re. At 1 month postoperatively, vascularzied neo-connective-tissue fibrils were found to fill the pores in the ECMs loaded with bFGF or ginsenoside Re. CONCLUSIONS: The aforementioned results indicated that like bFGF, ginsenoside Re-associated induction of angiogenesis enhanced tissue regeneration, supporting the concept of therapeutic angiogenesis in tissue-engineering strategies.

Study Seven
Roles of ginsenosides on morphine-induced hyperactivity and rewarding effect in mice.
Guo M, Wang JH, Yang JY, et al., Planta Med. 2004 Jul;70(7):688-90

Roles of ginsenosides on morphine-induced hyperactivity and rewarding effect in mice.

Guo M, Wang JH, Yang JY, et al., Planta Med. 2004 Jul;70(7):688-90

Ginsenosides, the main effective components of the root of Panax ginseng, have been reported to modulate morphine action. In the present study, ginsenosides Rd, Rb2, Rgl and Re were divided into two groups according to their effects in mice on morphine-induced hyperactivity and conditioned place preference (CPP). Ginsenosides Rd, Rb2, Rgl had no effect on morphine-induced hyperactivity, but antagonized morphine-induced CPP. On the contrary, ginsenoside Re increased morphine-induced hyperactivity whereas it showed no effect on morphine-induced CPP. Furthermore, Re antagonized the inhibitory effect of the mixture involving Rd, Rb2 and Rgl on the morphine action. These results suggest that ginsenosides with different structures have antagonizing properties in the regulation of morphine-induced reinforcement.

More studies on Rc (> 97 articles):

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Rc%20ginseng

More studies on Rd (> 105 articles):

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Rd%20ginseng

More studies on Re (> 153 articles):

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Search&db=pubmed&term=Re%20ginseng