• Preventive Nutrition and Food Science
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• v.8 no.1
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• pp.96-104
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• 2003

Ginger (Zingiber officinale Roscoe) is traditionally used as appetite enhancer, improver of the digestive system, antithusive, anti-cold, antipyretic, analgesic, and antiinflammation. In vitro evaluation using human lymphocyte cultures showed almost similar indication with those in in vivo mouse study, NK cell lysing activity was improved significantly. Proliferation activity of B and T cells, and CD3$^{＋}$ and CD3$^{＋}$CD4$^{＋}$T cell subset were better observed using oleoresin or gingerol and shogaol fractions. Although there were higher activities in gingerol, the improvement was almost equal to that by oleoresin. Shogaol did not show better improvement except at higher concentration. It could be concluded that treatment with single bioactive compound, such as gingerol, did not show significant effects compared to oleoresin, the crude extract. In human study, involving healthy male adult, the improvement of NK cell lysing activity was again demonstrated and even more apparent. The mechanism involved in the protection seemed to be through the antioxidant activity of gingerol. However, other mechanism underlying the improvement of NK cell lysing activity must be involved since this improvement seemed to be specifically toward NK cell activity. Since NK cells ave specific for the elimination of virus-infected cell and mutated cells, this positive effect on the immune system are very interesting. This work has also scientifically proved that the traditional beliefs that ginger had preventive effects on common cold appeared to be reasonable.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.1
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• pp.41-49
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• 2009

Soeumin-Googwihyangso-san(SGGHSS) has been used for the prevention or treatment of Soeumin-allergic rhinitis. This study was performed to demonstrate anti-allergic and anti-inflamatory effects of SGGHSS methanol extract in HMC cell lines and activated mouse B cells and CD4+ T cells. SGGHSS inhibited the production of TNF-$\alpha$ in PMA plus A23187 activated HMC-1 cells but not that of IL-6, as measured by ELISA. SGGHSS inhibited the expression of CD23 and surface IgE in B cells as determined by flowcytometry. It also inhibited secretion of IFN-$\gamma$ and IgG1, the Th1 related IgG type, but increased that of IL-4 in anti-CD40 and IL-4 treated B cells as measured by ELISA. As for Th cell differentiation, SGGHSS did not much affect IL-4 or IFN-$\gamma$. Taken together, our data showed that SGGHSS exerted an anti-inflammtory effect by inhibiting TNF-$\alpha$ in mast cells and has anti-allergic activity not via inhibition of CD4+ T cell, but via inhibition of B cells. These results suggest some evidence that SGGHSS can be applied to allergic disease.

• Biomolecules & Therapeutics
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• v.23 no.1
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• pp.39-44
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• 2015

Tolfenamic acid (TA) is a traditional non-steroid anti-inflammatory drug (NSAID) and has been broadly used for the treatment of migraines. Nuclear factor kappa B (NF-${\kappa}B$) is a sequence-specific transcription factor and plays a key role in the development and progression of inflammation and cancer. We performed the current study to investigate the underlying mechanisms by which TA suppresses inflammation focusing on NF-${\kappa}B$ pathway in TNF-${\alpha}$ stimulated human normal and cancer cell lines and lipopolysaccharide (LPS)-stimulated mouse macrophages. Different types of human cells (HCT116, HT-29 and HEK293) and mouse macrophages (RAW264.7) were pre-treated with different concentrations of TA and then exposed to inflammatory stimuli such as TNF-${\alpha}$ and LPS. Transcriptional activity of NF-${\kappa}B$, $l{\kappa}B-{\alpha}$-degradation, p65 translocation and mitogen-activated protein kinase (MAPK) activations were measured using luciferase assay and Western blots. Pre-treatment of TA repressed TNF-${\alpha}$- or LPS-stimulated NF-${\kappa}B$ transactivation in a dose-dependent manner. TA treatment reduced degradation of $l{\kappa}B-{\alpha}$ and subsequent translocation of p65 into nucleus. TA significantly down-regulated the phosphorylation of c-Jun N-terminal kinase (JNK). However, TA had no effect on NF-${\kappa}B$ signaling and JNK phosphorylation in HT-29 human colorectal cancer cells. TA possesses anti-inflammatory activities through suppression of JNK/NF-${\kappa}B$ pathway in different types of cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.9
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• pp.3901-3906
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• 2014

Aim: The purpose of this study was to investigate anti-tumor effects and safety of DH332, a new ${\beta}$-carboline alkaloids derivatives in vitro and in vivo. Materials and Methods: The effects of DH332 on human (RAMOS RA.1) and mouse (J558) B lymphoma cell lines were detected using a CCK-8 kit (Cell Counting Kit-8), and apoptosis was detected by flow cytometry with PI/annexinV staining. Western blotting was used to detected caspase-3 and caspase-8. Neurotoxic and anti-tumor effects were evaluated in animal experiments. Results: DH332 exerts a lower neurotoxicity compared with harmine. It also possesses strong antitumor effects against two B cell lymphoma cell lines with low $IC_{50s}$. Moreover, DH332 could inhibit the proliferation and induce the apoptosis of RAMOS RA.1 and J558 cell lines in a dose-dependent manner. Our results suggest that DH332 triggers apoptosis by mainly activating the caspase signaling pathway. In vivo studies of tumor-bearing BALB/c mice showed that DH332 significantly inhibited growth of J558 xenograft tumors. Conclusions: DH332 exerts effective antitumor activity in vitro and in vivo, and has the potential to be a promising drug candidate for lymphoma therapy.

• Journal of Ginseng Research
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• v.42 no.2
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• pp.133-143
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• 2018

Background: AD-2 (20(R)-dammarane-3b, 12b, 20, 25-tetrol; 25-OH-PPD) is a ginsenoside and isolated from Panax ginseng, showing anticancer activity against extensive human cancer cell lines. In this study, effects and mechanisms of 1C ((20R)-3b-O-(L-alanyl)-dammarane-12b, 20, 25-triol), a modified version of AD-2, were evaluated for its development as a novel anticancer drug. Methods: MTT assay was performed to evaluate cell cytotoxic activity. Cell cycle and levels of reactive oxygen species (ROS) were determined using flow cytometry analysis. Western blotting was employed to analyze signaling pathways. Results: 1C concentration-dependently reduces prostate cancer cell viability without affecting normal human gastric epithelial cell line-1 viability. In LNCaP prostate cancer cells, 1C triggered apoptosis via Bcl-2 family-mediated mitochondria pathway, downregulated expression of mouse double minute 2, upregulated expression of p53 and stimulated ROS production. ROS scavenger, N-acetylcysteine, can attenuate 1C-induced apoptosis. 1C also inhibited the proliferation of LNCaP cells through inhibition on $Wnt/{\beta}-catenin$ signaling pathway. Conclusion: 1C shows obvious anticancer activity based on inducing cell apoptosis by Bcl-2 family-mediated mitochondria pathway and ROS production, inhibiting $Wnt/{\beta}-catenin$ signaling pathway. These findings demonstrate that 1C may provide leads as a potential agent for cancer therapy.

• Korean Journal of Animal Reproduction
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• v.10 no.2
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• pp.168-174
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• 1986

These experiments were carried out to clarify the optimalconditions and interspecific cross reaction of H-Y antibody activity. H-Y antiserum was prepared in inbred SD female rats and Balb/c female mice by repeated immunization of rat newborn testis homogemate, rat and mouse spleen cells obtained from males of same strain. The activity of H-Y antibody in antiserum was tested by ELISA and biological tests. The cross reactivity of H-Y antibody was confirmed by culturing mouse and rabbit embryos in medium containing H-Y antibody and complement obtained from rat and guinea pig, respectively. The optimal condition for the activity of H-Y antibody was also investigated by culturing embryos in medium with different pH and complement concentration. The results obtained in these experiments were summarized as follows: 1. The formation rates of H-Y antibody in rats immunized with newborn testis and spleen cell were 40.0 and 50.0% respectively, and that in mouse immunized with spleen cell was 48.4%. 2. The activity of H-Y antibody was not affected by pH in range of 6.5 to 8.0, and the same was true for the relative concentration of complement to the H-Y antibody. 3. Minimum time needed for the activity of H-Y antibody was confirmed to be 0.5 to 1 hour and 24 to 48 hours respectively for the zona free embryos and intact embryos. 4. When mouse and rabbit embryos were treated with H-Y antibody obtained from rat, 46.4 and 54.8% of embryos were retarded or destroyed. From these results it could be said that H-Y antibody had strong interspecific cross reactivity.

• Toxicological Research
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• v.22 no.2
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• pp.95-102
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• 2006

Exposure to soluble nickel compound produces toxic effects on immune system, but the mechanism of action remains to be elucidated. Differential gene expression was studied to understand the potential molecular mechanism responsible for acute toxicity induced by nickel acetate in spleen cells. We exposed mouse spleen cells to nickel acetate with a nontoxic dose ($40{\mu}M$) and then extracted total RNA at 6 h and 12 h after exposure. The RNA was hybridized onto 10K mouse oligonucleotide microarrays, and data were analyzed using GeneSpring 7.1. Nickel had a modest effects on expression of many genes, in the range of 1.3-3 fold. The expression profile showed time-dependent changes in expression levels of differentially expressed genes, including some important genes related to cell cycle, apoptosis and DNA repair. In hierarchical cluster analysis of duplicate experiments, 111 genes were screened out. Out of these, 44 genes showing time- dependent up-regulation (>1.5 fold) and 38 genes showing down-regulation (>1.5 fold) at all time points were chosen for further analysis. The change in the expression of three genes (GPX1, GADD45B and FAIM) after nickel treatment was validated using RT-PCR. As a rule, a number of genes appear to be coordinately regulated between cell survival and cell death from nickel toxicity. In conclusion, changes in the gene profile in the spleen after nickel treatment are complex and genes with diverse functions are modulated. These findings will be contributed to the understanding of the complicated biological effects of nickel.

• BMB Reports
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• v.55 no.12
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• pp.633-638
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• 2022

Liver regeneration is a well-known systemic homeostatic phenomenon. The N⁶-methyladenosine (m⁶A) modification pathway has been associated with liver regeneration and hepatocellular carcinoma. m⁶A methyltransferases, such as methyltransferase 3 (METTL3) and methyltransferase 14 (METTL14), are involved in the hepatocyte-specific-regenerative pathway. To illustrate the role of METTL14, secreted from non-parenchymal liver cells, in the initiation phase of liver regeneration, we performed 70% partial hepatectomy (PH) in Mettl14 heterozygous (HET) and wild-type (WT) mice. Next, we analyzed the ratio of liver weight to body weight and the expression of mitogenic stimulators derived from non-parenchymal liver cells. Furthermore, we evaluated the expression of cell cycle-related genes and the hepatocyte proliferation rate via MKI67-immunostaining. During regeneration after PH, the weight ratio was lower in Mettl14 HET mice compared to WT mice. The expressions of hepatocyte growth factor (HGF) and tumor necrosis factor (TNF)-α, mitogens derived from non-parenchymal liver cells that stimulate the cell cycle, as well as the expressions of cyclin B1 and D1, which regulate the cell cycle, and the number of MKI67-positive cells, which indicate proliferative hepatocyte in the late G1-M phase, were significantly reduced in Mettl14 HET mice 72 h after PH. Our findings demonstrate that global Mettl14 mutation may interrupt the homeostasis of liver regeneration after an acute injury like PH by restraining certain mitogens, such as HGF and TNF-α, derived from sinusoidal endothelial cells, stellate cells, and Kupffer cells. These results provide new insights into the role of METTL14 in the clinical treatment strategies of liver disease.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.25 no.4 s.34
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• pp.133-143
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• 1999

To identify inhibitory effect of Bamboo extract on melanogenesis, the effect was compared with arbutin, ascorbic acid, hydroquinone, and kojic acid on the melanin biosynthesis in B16 mouse melanoma cells and cultured human melanocytes. The cell viability of the agent was tested on cultured human melanocytes. We also examined its. free radical scavenging activity on 1,1-diphenyl-2-picrylhydrazyl(DPPH). Bamboo extract showed considerable effect against melanin production and did not reduce cell viability at the concentration tested. It also showed potent free radical scavenging activity.

• The Journal of Korean Obstetrics and Gynecology
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• v.22 no.3
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• pp.66-82
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• 2009

Purpose: This study was performed to elucidate the inhibitory effect of Yukmijihwangtang-gagambang (YMG) on melanin synthesis in B16F10 mouse melanoma cell. Methods: To demonstrate the inhibitory effects of YMG on melanin synthesis, we measured the amount of released and produced melanin in B16F10 melanoma cell. Also, we evaluated tyrosinase-activity in vitro as well as in B16F10 melanoma cell. And to investigate the action mechanism we assessed the gene expressions of tyrosinase, TRP-1, TRP-2, MMP-2, PKA, PKC${\beta}$, ERK-1 ERK-2, AKT-1 and MITF in B16F10 melanoma cells. Results: 1. YMG decreased the release and production of melanin in B16F10 melanoma cells. 2. YMG decreased tyrosinase activity in vitro and in B16F10 melanoma cells. 3. YMG decreased the expression of tyrosinase, TRP-1, TRP-2, PKA, PKC${\beta}$ and MMP-2 in B16F10 melanoma cells. 4. YMG increased the expression of ERK-1, ERK-2, and AKT-1 in B16F10 melanoma cells. 5. YMG decreased the expression of MITF in B16F10 melanoma cells. Conclusion: From these results, we suggest that YMG inhibit melanin synthesis via tyrosinase inhibition and regulation of the gene expression in B16F10 melanoma cells.