• Journal of Ginseng Research
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• v.25 no.1
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• pp.45-52
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• 2001

The storage stability of fresh ginseng packaged individually in a soft film bag was more enhanced as the soft film with lower oxygen permeability was used, while the optimum water vapor permeability for enhancing the storage stability of fresh ginseng was estimated 3.5 g/m$^2$$.$day$.$90% RH when using the soft film with low oxygen permeability of 3.6∼5.4 cc/m$^2$$.$day$.$atm. The storage stability of the individually packaged fresh ginseng was also enhanced when the soft film bag was filled with carbon dioxide-oxygen-nitrogen (25:5:70) miked gas but the vacuum packaging exhibited little effect for the enhancement of storage stability of the fresh ginseng.

• Journal of Ginseng Research
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• v.42 no.4
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• pp.455-462
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• 2018

Background: Ginsenoside Rh2 has been known to enhance the activity of immune cells, as well as to inhibit the growth of tumor cells. Although the repertoire of genes regulated by Rh2 is well-known in many cancer cells, the epigenetic regulation has yet to be determined, especially for comprehensive approaches to detect methylation changes. Methods: The effect of Rh2 on genome-wide DNA methylation changes in breast cancer cells was examined by treating cultured MCF-7 with Rh2. Pyrosequencing analysis was carried out to measure the methylation level of a global methylation marker, LINE1. Genome-wide methylation analysis was carried out to identify epigenetically regulated genes and to elucidate the most prominent signaling pathway affected by Rh2. Apoptosis and proliferation were monitored to examine the cellular effect of Rh2. Results: LINE1 showed induction of hypomethylation at specific CpGs by 1.6-9.1% (p < 0.05). Genome-wide methylation analysis identified the "cell-mediated immune response"-related pathway as the top network. Cell proliferation of MCF-7 was retarded by Rh2 in a dose-dependent manner. Hypermethylated genes such as CASP1, INSL5, and OR52A1 showed downregulation in the Rh2-treated MCF-7, while hypomethylated genes such as CLINT1, ST3GAL4, and C1orf198 showed upregulation. Notably, a higher survival rate was associated with lower expression of INSL5 and OR52A1 in breast cancer patients, while with higher expression of CLINT1. Conclusion: The results indicate that Rh2 induces epigenetic methylation changes in genes involved in immune response and tumorigenesis, thereby contributing to enhanced immunogenicity and inhibiting the growth of cancer cells.

• 한국약용작물학회:학술대회논문집
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• 2007.11a
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• pp.287.2-287.2
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• 2007

• Journal of Ginseng Research
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• v.46 no.3
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• pp.396-407
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• 2022

Background: Colorectal cancer (CRC) has a high morbidity and mortality worldwide. 20 (S)-ginsenoside Rh2 (G-Rh2) is a natural compound extracted from ginseng, which exhibits anticancer effects in many cancer types. In this study, we demonstrated the effect and underlying molecular mechanism of G-Rh2 in CRC cells in vitro and in vivo. Methods: Cell proliferation, migration, invasion, apoptosis, cell cycle, and western blot assays were performed to evaluate the effect of G-Rh2 on CRC cells. In vitro pull-down assay was used to verify the interaction between G-Rh2 and Axl. Transfection and infection experiments were used to explore the function of Axl in CRC cells. CRC xenograft models were used to further investigate the effect of Axl knockdown and G-Rh2 on tumor growth in vivo. Results: G-Rh2 significantly inhibited proliferation, migration, and invasion, and induced apoptosis and G₀/G₁ phase cell cycle arrest in CRC cell lines. G-Rh2 directly binds to Axl and inhibits the Axl signaling pathway in CRC cells. Knockdown of Axl suppressed the growth, migration and invasion ability of CRC cells in vitro and xenograft tumor growth in vivo, whereas overexpression of Axl promoted the growth, migration, and invasion ability of CRC cells. Moreover, G-Rh2 significantly suppressed CRC xenograft tumor growth by inhibiting Axl signaling with no obvious toxicity to nude mice. Conclusion: Our results indicate that G-Rh2 exerts anticancer activity in vitro and in vivo by suppressing the Axl signaling pathway. G-Rh2 is a promising candidate for CRC prevention and treatment.

• Journal of the Korean Society of Food Science and Nutrition
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• v.41 no.8
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• pp.1151-1157
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• 2012

This study was conducted to investigate methods of increasing raw ginseng consumption. To accomplish this, Insambob was prepared by adding minced raw ginseng (MRG), ground raw ginseng (GRG) or extracts of red ginseng (RGE). Sensory quality, textural properties, and changes in the ginsenoside and free amino acid composition of the Insambob then were investigated. Insambob containg 50% RGE had the best color, flavor and texture, but that containing 10% GRG had the best taste and overall acceptability. The hardness and adhesiveness were highest for containing 10% GRG and decreased as the amount of ginseng added increased. However, the hardness increased, while the adhesiveness of Insambob containg RGE decreased significantly as the amount added increased. Moreover, the ginsenoside composition changed upon addition of ginseng, with the levels of ginsenoside-Rb1, -Rb2, -Rb3, -Rc, -Re, -Rd, -Rg1, and -Rf decreasing and ginsenoside-Rh2, -Rh1, and -Rg3 newly appearing. Finally, the total free amino acid contents of Insambob increased upon addition of MRG, GRG and RGE.

• Journal of Ginseng Research
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• v.21 no.3
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• pp.147-152
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• 1997

Ginsenosides $Rh_1$ and $Rh_2$ Induced the differentiation of F9 teratocarcinoma stem cells. These agents are structurally similar to the steroid hormones, therefore, we speculated that the steroid receptor (s) or novel nuclear receptor (s) could be involved in the differentiation process induces by them. Based on this speculation, we tried to alone new nuclear receptors with reverse transcription-polymerase chain reaction (RT-PCR) method by isolating RNA from F9 teratocarcinoma cells induced by ginsenosides. By using RT-PCR with degenerated primers from highly conserved DNA binding domain of nuclear receptors, we identified several nuclear receptors. In northern blot analysis we found that these clones are transcriptionally regulated by ginsenoside Rhl or Rh2 treatment. Further characterizations of these clones are needed to identify the mechanism of gene expression, which has an important role in the differentiation of F9 cells induced by ginsenosides.

• Archives of Pharmacal Research
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• v.27 no.4
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• pp.429-435
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• 2004

Ginseng has an anti-cancer effect in several cancer models. This study was to characterize active constituents of ginseng and their effects on proliferation of prostate cancer cell lines, LNCaP and PC3. Cell proliferation was measured by $[^3H]$thymidine incorporation, the intracellular calcium concentration by a dual-wavelength spectrophotometer system, effects on mite-gen-activated protein (MAP) kinases by Western blotting, and cell attachment and morphologic changes were observed under a microscope. Among 11 ginsenosides tested, ginsenosides $Rg_3\;and\;Rh_2$ inhibited the proliferation of prostate cancer cells. $EC_{50}s\;of\;Rg_3\;and\;Rh_2$ on PC3 cells were $8.4{\mu}M\;and\;5.5{\mu}M$, respectively, and $14.1{\mu}M\;and\;4.4{\mu}M$ on LNCaP cells, respectively. Both ginsenosides induced cell detachment and modulated three modules of MAP kinases activities differently in LNCaP and PC3 cells. These results suggest that ginsenosides $Rg_3\;and\;Rh_2$-induced cell detachment and inhibition of the proliferation of prostate cancer cells may be associated with modulation of three modules of MAP kinases.

• 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.

• Journal of the Korean Society of Food Science and Nutrition
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• v.39 no.8
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• pp.1194-1200
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• 2010

This study was carried out to investigate the compositional changes of ginsenosides and phenolic acids of ginseng leaf by fermentation in order to promote the utilization of ginseng leaf. The chief ginsenosides in non-fermented ginseng leaf (NFGL) were ginsenoside-Rg1 (26.0 mg/g), -Re (47.3 mg/g) and -Rd (23.9 mg/g). By fermentation, ginsenoside-Rg1, -Rb1, -Rb2, -Rb3, -Rc and -Re were decreased tremendously and new ginsenoside-Rh2, -Rh1, -Rg2 and -Rg3 appeared. Especially, ginsenoside-Rg3 (3.7 mg/g) on FGL was increased 15-fold compared to that of NFGL (0.2 mg/g). Total phenolic compound content of NFGL and FGL measured by colorimetric analysis was 350.4 and 312.5 mg%, respectively. There were 8 free and 6 ester forms of phenolic acids in NFGL. Among them, content of ferulic acid was the highest, comprised of 12.6 and 50.7 mg%, respectively. In FGL, total content of protocatechuic acid, p-hydroxybenzoic acid, and vanillic acid were increased by 28, 5 and 7.8 fold and ferulic acid was decreased greatly. Tyrosinase inhibitory activity of FGL was stronger than NFGL, while electron donating abilities of FGL were similar to NFGL.

• Journal of Ginseng Research
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• v.44 no.2
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• pp.274-281
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• 2020

Background: Ultraviolet (UV) goes through the epidermis and promotes release of inflammatory cytokines in keratinocytes. Granulocyte-macrophage colony-stimulating factor (GM-CSF), one of the keratinocyte-derived cytokines, regulates proliferation and differentiation of melanocytes. Extracellular signal-regulated kinase (ERK1/2) and protein kinase C (PKC) signaling pathways regulate expression of GM-CSF. Based on these results, we found that ginsenoside Rh3 prevented GM-CSF production and release in UV-B-exposed SP-1 keratinocytes and that this inhibitory effect resulted from the reduction of PKCδ and ERK phosphorylation. Methods: We investigated the mechanism by which ginsenoside Rh3 from Panax ginseng inhibited GM-CSF release from UV-B-irradiated keratinocytes. Results: Treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) or UV-B induced release of GM-CSF in the SP-1 keratinocytes. To elucidate whether the change in GM-CSF expression could be related to PKC signaling, the cells were pretreated with H7, an inhibitor of PKC, and irradiated with UV-B. GM-CSF was decreased by H7 in a dose-dependent manner. When we analyzed which ginsenosides repressed GM-CSF expression among 15 ginsenosides, ginsenoside Rh3 showed the largest decline to 40% of GM-CSF expression in enzyme-linked immunosorbent assay. Western blot analysis showed that TPA enhanced the phosphorylation of PKCδ and ERK in the keratinocytes. When we examined the effect of ginsenoside Rh3, we identified that ginsenoside Rh3 inhibited the TPA-induced phosphorylation levels of PKCδ and ERK. Conclusion: In summary, we found that ginsenoside Rh3 impeded UV-B-induced GM-CSF production through repression of PKCδ and ERK phosphorylation in SP-1 keratinocytes.