• Journal of Microbiology and Biotechnology
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• v.16 no.11
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• pp.1791-1798
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• 2006

When ginsenoside Rg5, a main component isolated from red ginseng, was incubated with three human fecal microflora for 24 h, all specimens showed hydrolyzing activity: all specimens produced ginsenoside Rh3 as a main metabolite, but a minor metabolite $3{\beta},12{\beta}$-dihydroxydammar-21(22),24-diene (DD) was observed in two specimens. To evaluate the antiallergic effect of ginsenoside Rg5 and its metabolites, the inhibitory effect of ginsenoside Rg5 and its metabolite ginsenoside Rh3 against RBL-2H3 cell degranulation, mouse passive cutaneous anaphylaxis (PCA) reaction induced by the IgE-antigen complex, and mouse ear skin dermatitis induced by 12-O-tetradecanoilphorbol-13-acetate (TPA) were measured. Ginsenosides Rg5 and Rh3 potently inhibited degranulation of RBL-2H3 cells. These ginsenosides also inhibited mRNA expression of proinflammatory cytokines IL-6 and $TNF-{\alpha}$ in RBL-2H3 cells stimulated by IgE-antigen. Orally and intraperitoneally administered ginsenoside Rg3 and orally administered ginsenoside Rg5 to mice potently inhibited the PCA reaction induced by IgE-antigen complex. However, intraperitoneally administered ginsenoside Rg5 nearly did not inhibit the PCA reaction. These ginsenosides not only suppressed the swelling of mouse ears induced by TPA, but also inhibited mRNA expression of cyclooxygenase-2, $TNF-{\alpha}$, and IL-4 and activation of transcription factor NF-kB. These inhibitions of ginsenoside Rh3 were more potent than those of ginsenoside Rg5. These findings suggest that ginsenoside Rg5 may be metabolized in vivo to ginsenoside Rh3 by human intestinal microflora, and ginsenoside Rh3 may improve antiallergic diseases, such as rhinitis and dermatitis.

• YAKHAK HOEJI
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• v.35 no.5
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• pp.432-437
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• 1991

A mixture of 20(R)- and 20(S)-ginsenoside Rg$_{3}$ was obtained under mild acidic hydrolysis from protopanaxadiol saponins, ginsenosides Rb$_{1}$, Rb$_{2}$, Rc and Rd. The product was acetylated to give the peracetates, which were further converted into 20(R)-ginsenoside Rg$_{3}$, 20(S)-ginsenoside Rg$_{3}$, 20(R)-ginsenoside Rh$_{2}$ and 20(S)-ginsenoside Rh$_{2}$ by the direct alkaline treatment depending upon two kinds of temperature conditions respectively. The structure and physicochemical properties of a prosapogenin, 20(R)-ginsenoside Rh$_{2}$, were investigated.

• Archives of Pharmacal Research
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• v.27 no.1
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• pp.61-67
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• 2004

When ginseng water extract was incubated at $60^{\circ}C$ in acidic conditions, its protopanaxadiol ginsenosides were transformed to ginsenoside $Rg_3$ and ${\Delta}^{20}$-ginsenoside $Rg_3$. However, protopanaxadiol glycoside ginsenosides $Rb_1, Rb_2$ and Rc isolated from ginseng were mostly not transformed to ginsenoside $Rg_3$ by the incubation in neutral condition. The transformation of these ginsenosides to ginsenoside $Rg_3$ and ${\Delta}^{20}$-ginsenoside $Rg_3$ was increased by increasing incubation temperature and time in acidic condition: the optimal incubation time and temperature for this transformation was 5 h and $60^{\circ}C$ resepectively. The transformed ginsenoside $Rg_3$ and ${\Delta}^{20}$-ginsenoside $Rg_3$ were metabolized to ginsenoside $Rh_2$ and $\Delta^{20}$--ginsenoside $Rh_2$, respectively, by human fecal microflora. Among the bacteria isolated from human fecal microflora, Bacteroides sp., and Bifidobacterium sp. and Fusobacterium sp. potently transformed ginsenoside $Rg_3$ to ginsenoside $Rh_2$. Acid-treated ginseng (AG) extract, fermented AG extract, ginsenoside $Rh_2$ and protopanaxadiol showed potent cytotoxicity against tumor cell lines. AG extract, fermented AG extract and protopanaxadiol potently inhibited the growth of Helicobacter pylori.

• BMB Reports
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• v.56 no.10
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• pp.551-556
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• 2023

Ginsenosides, among the most active components of ginseng, exhibit several therapeutic effects against cancer, diabetes, and other metabolic diseases. However, the molecular mechanism underlying the anti-osteoporotic activity of ginsenoside Rg2, a major ginsenoside, has not been clearly elucidated. This study aimed to determine the effects of ginsenoside Rg2 on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation. Results indicate that ginsenoside Rg2 inhibits RANKL-induced osteoclast differentiation of bone marrow macrophages (BMMs) without cytotoxicity. Pretreatment with ginsenoside Rg2 significantly reduced the RANKL-induced gene expression of c-fos and nuclear factor of activated T-cells (Nfatc1), as well as osteoclast-specific markers tartrate-resistant acid phosphatase (TRAP, Acp5) and osteoclast-associated receptor (Oscar). Moreover, RANKL-induced phosphorylation of mitogen-activated protein kinases (MAPKs) was decreased by ginsenoside Rg2 in BMM. Therefore, we suggest that ginsenoside Rg2 suppresses RANKL-induced osteoclast differentiation through the regulation of MAPK signaling-mediated osteoclast markers and could be developed as a therapeutic drug for the prevention and treatment of osteoporosis.

• Journal of Ginseng Research
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• v.32 no.3
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• pp.264-269
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• 2008

Ginsenosides are major components in Panax ginseng and known to have numerous pharmacological activities such as anti-cancer, anti-diabetes, anti-viral and anti-atherosclerosis effects. In this study, the regulatory activities of G-Rg3 and its derivative 25-hydroxy Rg3 (G-Rg3-2H) on the production of nitric oxide (NO) in macrophages and the proliferation of lymphocytes prepared from spleen and bone marrow under treatment of lipopolysaccharide (LPS) or concanavalin (Con) A were examined. G-Rg3 and G-Rg3-2H dose-dependently inhibited NO production from LPS-activated RAW264.7 cells and in agreement, these compounds protected RAW264.7 cells from LPS-mediated cytotoxicity. In contrast, G-Rg3-2H dose-dependently inhibited lymphocyte proliferation induced by both LPS and Con A, while there was no inhibition by G-Rg3. Therefore, our data suggest that these compounds may be applied for NO-mediated or lymphocyte-mediated immunological diseases.

• Journal of Ginseng Research
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• v.45 no.6
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• pp.654-664
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• 2021

Background: Ginsenoside Rg3, isolated from Panax ginseng, has anti-inflammatory and anti-tumor activities. It is known to reduce inflammation in acute lung injury in mice, and to reduce the expression of inflammatory cytokines and COX-2 in human asthmatic airway epithelium. In this study, we attempted to determine whether ginsenoside Rg3 inhibits airway inflammation, oxidative stress, and airway hyperresponsiveness (AHR) in the lungs of asthmatic mice. We also investigated its effects on oxidative stress and the inflammatory response in tracheal epithelial cells. Methods: Asthma symptoms were induced in female BALB/c mice sensitized with ovalbumin (OVA). Mice were divided into five groups: normal controls, OVA-induced asthmatic controls, and asthmatic mice treated with ginsenoside Rg3 or prednisolone by intraperitoneal injection. Inflammatory BEAS-2B cells (human tracheal epithelial cells) treated with ginsenoside Rg3 to investigate its effects on inflammatory cytokines and oxidative responses. Results: Ginsenoside Rg3 treatment significantly reduced eosinophil infiltration, oxidative responses, airway inflammation, and AHR in the lungs of asthmatic mice. Ginsenoside Rg3 reduced Th2 cytokine and chemokine levels in bronchoalveolar lavage fluids and lung. Inflammatory BEAS-2B cells treated with ginsenoside Rg3 reduced the eotaxin and pro-inflammatory cytokine expressions, and monocyte adherence to BEAS-2B cells was significantly reduced as a result of decreased ICAM-1 expression. Furthermore, ginsenoside Rg3 reduced the expression of reactive oxygen species in inflammatory BEAS-2B cells. Conclusion: Ginsenoside Rg3 is a potential immunomodulator that can ameliorate pathological features of asthma by decreasing oxidative stress and inflammation

• Archives of Pharmacal Research
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• v.29 no.8
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• pp.685-690
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• 2006

The effect of a main constituent ginsenoside Rg5 isolated from red ginseng and its metabolite ginsenoside Rh3 in a chronic dermatitis model was investigated. Ginsenosides Rg5 and Rh3 suppressed swelling of oxazolone-induced mouse ear contact dermatitis. These ginsenosides also reduced mRNA expressions of cyclooxygenase-2, interleukin $(IL)-1{\beta}$, tumor necrosis factor $(TNF)-{\alpha}$ and interferon $(IFN)-{\gamma}$. The inhibition of ginsenoside Rh3 was more potent than that of ginsenoside Rg5. These findings suggest that ginsenoside Rh3 metabolized from ginsenoside Rg5 may improve chronic dermatitis or psoriasis by the regulation of $IL-1{\beta}$ and $TNF-{\alpha}$ produced by macrophage cells and of $IFN-{\gamma}$ produced by Th cells.

• Mycobiology
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• v.38 no.2
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• pp.153-155
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• 2010

To produce ginsenoside-$Rg_3$ enriched yeast from ginseng-steaming effluent (GSE), Lipomyces starkeyi, which tends to grow well in GSE, was cultured in sterilized GSE and its growth and production of ginsenoside-$Rg_3$ were determined. Growth of L. starkeyi was 86.1 mg per g GSE and its ginsenoside-$Rg_3$ contents was 0.013 mg per g GSE.

• Journal of Microbiology and Biotechnology
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• v.28 no.3
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• pp.391-396
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• 2018

It is well known that Korean red ginseng has various biological activities. However, there is little knowledge about the antiviral activity of Korean red ginseng and its ginsenosides. In this study, we addressed whether oral administration of ginsenoside-Rb2 and -Rg3 is able to protect against rotavirus (RV) infection. The protective effect of ginsenosides against RV infection was examined using an in vivo experiment model in which newborn mice (10-day-old) were inoculated perorally (p.o.) with $1.5{\times}10^6$ plaque-forming units/mouse of RV strain SA11. When various dosages of ginsenoside-Rb2 (25-250 mg/kg) were administered 3days, 2 days, or 1 day before virus challenge, treatment with this ginsenoside at the dosage of 75 mg/kg 3days before virus infection most effectively reduced RV-induced diarrhea. In addition, consecutive administration of ginsenoside-Rb2 (75 mg/kg) at 3 days, 2 days, and 1 day before virus infection was more effective than single administration on day -3. The consecutive administration of ginsenoside-Rb2 also reduced virus titers in the bowels of RV-infected mice. In an experiment to compare the protective activity between ginsenoside-Rb2 and its two hydrolytic products (20(S)- and 20(R)-ginsenoside-Rg3), 20(S)-ginsenoside-Rg3, but not 20(R)-ginsenoside-Rg3, prevented RV infection. These results suggest that ginsenoside-Rb2 and its hydrolytic product, 20(S)-ginsenoside-Rg3, are promising candidates as an antiviral agent to protect against RV infection.

• Korean Journal of Plant Resources
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• v.19 no.1
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• pp.139-143
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• 2006

To increase the contents of functional ginsenosides by conversion, especially ginsenoside-$Rg_3$ and $Rh_2$, the extracts of red ginseng were treated with high temperature and citric acid or apricot extract. When the extracts were subject to $120^{\circ}C$ for 2 hours, the content of ginsenoside-$Rg_3$ was increased 2 times than in control. When the extracts were subject to $120^{\circ}C$ and acidic conditions adjusted with citric acid, the ginsenoside-$Rg_3$, was detected 2.8 times, but other ginsenoside were decreased heavily to 65%. When the extract were treated with for 12 hours at $80^{\circ}C$, the content of ginsenoside-$Rg_3$ was increased to 3.3 times, Also, when the red ginseng extracts were treated with apricot extract, the ginsenoside-$Rg_3$ was detected to 4 times than in control, but other ginsenoside were decreased lightly to 35%, not same as at the $120^{\circ}C$ treatment.