• Proceedings of the PSK Conference
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• 2000.10a
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• pp.192.3-193
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• 2000

• Journal of Applied Biological Chemistry
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• v.43 no.1
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• pp.59-61
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• 2000

The cytotoxic activities of the methanol extracts of 44 plant species in 31 families against five human solid A549 (lung), SK-OV-2 (ovarian), SK-MEL-2 (melanoma), XF-498 (central nervous system), and HCT-15 (colon) tumor cell lines were examined using the sulforhodamine B (SRB) assay. Responses varied with both cell line and plant species used. Potent cytotoxic activities ($ED_{50}$, <$40{\mu}g/ml$) against all model tumor cell lines were produced from the extracts of Rhus chinensis gall (Galla rhois), Betula platyphylla var. japonica bark, Inula helenium root, Cinnamomum cassia bark, Cinnamomum sieboldii root bark, Lysimachia davurica whole plant, and Evodia rutaecarpa fruit. These plants may be useful for developing new types of naturally occurring anti-tumor agents.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.2 no.1
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• pp.25-42
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• 1996

In order to study the effect of Sikbuntang on the in vitro Cell-cytotoxicity, this study had put through MTT Assay. And to investigate the effects of Sikbuntang on the ICR mice which had Abdominal tumor induced by Sarcoma-180 cell line, C57Bl/6 mice which had pulmonary melanoma induced by B16 cell line. After Sarcoma-180 cell line and B16 cell line were transplanted, the extract of Sikbuntang was orally administered to the mice to observe the extension of survival time of the mice, inhibition of solid tumor, inhibition of pulmonary melanoma metastasis, productivity of Interleukin-2, NK-Activity. The results were summarized as follows : 1. On the MTT assay, in case of $100{\mu}g/ml$ and $10{\mu}g/ml$ of Sikbuntang concentration were inhibited cell viability significantly. But $1{\mu}g/ml$ of Sikbuntang concentration just had tend to inhibit cell viability. 2. In the effect of life extension, Sikbuntang treated group appeared to survive longer than the control group, but which were not significant. 3. In the effect of inhibition solid tumor, Sikbuntang treated group appeared to decrease than the control group, but which were not significant. 4. In the effect of inhibition melanoma pulmonary metastasis, Sikbuntang treated group appeared to inhibit than the control group significantly. 5. In the productivity of Interleukin-2, on 7 and 14 day, Sikbuntang treated group increased than control group significantly. But on 21 day, Sikbuntang treated group had tend to increase with no significance. 6. In the NK-Activity, the ratio of effector cell and target cell. In case which the ratio was 50:1, Sikbuntang treated group showed increase than control group significantly. But in another cases, they showed increase with no significance.

• The Journal of Dong Guk Oriental Medicine
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• v.9
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• pp.139-154
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• 2000

This studies were examined in orther to investigate the object and the method of animal experimental papers on medicinal herbs of cancer therapeutic activities from the reported 23 literatures containing anti-cancer effects of medicinal herbs. The results were obtained as follows: 1. The oriental medicinal therapies on cancer were Pujeung(扶正法), Kuesa(祛邪法), Pujeungkuesa(扶正法邪法). 2. The experimental medicinal herbs of cancers therapy were 103 species, which was used for experimental cancer single or combine. Among then, Houttuyniae herba, Polyporus, Manitis squama, Evodiae fructus, Aucklandiae radix and Pharbitidis semen were effective for cancer treatment, while Houttuyniae herba inhibited tumor cells, but not normal cells. Also, Evodiae fructus, Aucklandiae radix and Pharbitidis semen showed strong cytoxicities on 20 different tumor cell lines, whereas Saururi herba seu rhizoma showed cytoxicity against HT-29 cell, melanoma, SK-MEL-5 cell, and Anemarrhenae rhizoma against ovarian tumor cell only, and Schizonepetae herba against HT-29 cell line only with a potent inhivitory activities. 3. P815 cell, Yac-1 cell, Sarcoma 180 cell, K 562 cell, and SNU-1 cells were frequently used as experimental cancer therapy.

• Journal of Ginseng Research
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• v.45 no.1
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• pp.98-107
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• 2021

Background: Ginseng extracts and ginseng-fermented products are widely used as functional cosmetic ingredients for their whitening and antiwrinkle effects. Recently, increasing attention has been given to bioactive metabolites isolated from endophytic fungi. However, little is known about the bioactive metabolites of the fungi associated with Panax ginseng Meyer. Methods: An endophytic fungus, Penicillium sp. SNF123 was isolated from the root of P. ginseng, from which acremonidin E was purified. Acremonidin E was tested on melanin synthesis in the murine melanoma cell line B16F10, in the human melanoma cell line MNT-1, and in a pigmented 3D-human skin model, Melanoderm. Results: Acremonidin E reduced melanogenesis in α-melanocyte-stimulating hormone (α-MSH)-stimulated B16F10 cells with minimal cytotoxicity. qRT-PCR analysis demonstrated that acremonidin E downregulated melanogenic genes, including tyrosinase and tyrosinase-related protein 1 (TRP-1), while their enzymatic activities were unaffected. The antimelanogenic effects of acremonidin E were further confirmed in MNT-1 and a pigmented 3D human epidermal skin model, Melanoderm. Immunohistological examination of the Melanoderm further confirmed the regression of both melanin synthesis and melanocyte activation in the treated tissue. Conclusion: This study demonstrates that acremonidin E, a bioactive metabolite derived from a fungal endophyte of P. ginseng, can inhibit melanin synthesis by downregulating tyrosinase, illuminating the potential utility of microorganisms associated with P. ginseng for cosmetic ingredients.

• International Journal of Oral Biology
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• v.36 no.3
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• pp.155-162
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• 2011

Eugenol (4-allyl-2-methoxyphenol) is a naturally occurring phenolic compound that is widely used in dentistry as a component of zinc oxide eugenol cement that is commonly applied to the mouth environment. Cisplatin is one of the most potent known anticancer agents and shows significant clinical activity against a variety of solid tumors. This study was undertaken to investigate the synergistic apoptotic effects of co-treatments with eugenol and cisplatin on human melanoma (G361) cells. To investigate whether this co-treatment efficiently reduces the viability of G361 cells compared with each single treatment, an MTT assay was conducted. The induction and augmentation of apoptosis were confirmed by DNA electrophoresis, Hoechst staining and an analysis of DNA hypoploidy. Western blot analysis and immunofluorescent staining were also performed to evaluate the expression levels and the translocation of apoptosis-related proteins following this co-treatment. Furthermore, proteasome activity and mitochondrial membrane potential (MMP) changes were also assayed. The results indicated that a co-treatment with eugenol and cisplatin induced multiple pathways and processes associated with an apoptotic response in G361 cells including nuclear condensation, DNA fragmentation, a reduction in MMP and proteasome activity, the increase and decrease of Bax and Bcl-2, a decreased DNA content, the release of cytochrome c into the cytosol, the translocation of AIF and DFF40 (CAD) into the nucleus, and the activation of caspase-9, caspase-7, caspase-3, PARP and DFF45 (ICAD). In contrast, separate treatments of 300 ${\mu}M$ eugenol or 3 ${\mu}M$ cisplatin for 24 h did not induce apoptosis. Our present data thus suggest that a combination therapy of eugenol and cisplatin is a potential treatment strategy for human melanoma.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.2 no.1
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• pp.57-73
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• 1996

These studies were consist of two sub-experiment. In order to study the effect of Banhahubaktang on the Cell-cytotoxicity In vitro. We had put through MTT Assay. In order to investigate the effects of Banhahubaktang on the ICR mice which had Abdominal tumor induced by Sarcoma-180 cell line, C57BL/6 mice which had pulmonary melanoma induced by B16 cell line. After Sarcoma-180 cell line and B16 cell line were transplanted, the extract of Banhahubaktang was orally administered to the mice to observe the extension of survival time of the mice, inhibition of solid tumor, inhibition of pulmonary melanoma metastasis. productivity of Interleukin-2, NK-Activity. The results were summarized as follows: 1. On the MTT assay, in case of $100{\mu}g/ml$ and $10{\mu}g/ml$ of Banhahubaktang concentration were inhibited cell viability significantly. But $1{\mu}g/ml$ of Banhahubaktang was tended to inhibit cell viability with no significance. 2. In the effect of life extension, Banhahubaktang treated group appeared to survive longer than the control group, but which were not significant. 3. In the effect of inhibit solid tumor, Banhahubaktang treated group appeared to decrease than the control group, but which were not significant. 4. In the effect of inhibit melanoma pulmonary metastasis. Banhahubaktang treated group appeared to inhibit than the control group significantly. 5. In the productivity of Interleukin-2, on 7 and 14 day, Banhahubaktang treated group increased than control group, which were significant. But on 21 day, test group and control group were much in common. 6. In the NK-Activity, Banhahubaktang treated group and control group were much in common.

• Journal of Digital Convergence
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• v.15 no.11
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• pp.285-295
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• 2017

This study aims to provide basic data on useful functional ingredients in red ginseng by studying the anti-inflammatory and anti-cancer effects of convergence of ginsenoside Rh2(Rh2) and compound K(CK) isolated from amplified red ginseng. Therefore we examined cytotoxicity in Hep3B, activity of IL-6 induced STAT3 luciferase and survival concentration of cells in B16F10 and HaCa T. According to the experimental results, when the Rh2 and CK mixture were 10 ug/ml, there was no cytotoxicity in Hep3B cells and the anti-inflammatory effect of IL-6 reduction ratio was 102%. In addition, Rh2 and CK mixture were observed to be toxic in melanoma cell line B16F10 and HaCa T (human keratinocyte) at 50 uM. FACS(fluorescence activated cell sorting) analysis showed that annexin V was not expressed and melanoma cells and keratinocyte were desorbed and killed. It can be assumed that the mechanism of killing through this phenomenon is due to the cell death of anoikis-type, and it is necessary to study the changes of cell adhesion proteins in the future in order to clarify the cell death signal system.

• Journal of Acupuncture Research
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• v.18 no.1
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• pp.129-145
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• 2001

Objectives : To characterize the antitumorigenic potential of three representative bee venom components, Melittin, Apamin, and Phospholipase A2, their effects on cell proliferation and apotosis of the human melanoma cell line SK-MEL-2 were analyzed using molecular biological approaches. Methodes & Results : To determine the doses of the drugs that do not induce cytotoxic damage to this cell line, cell viability was examined by MTT assay. While SK-MEL-2 cells treated with 0.5 - 2.0㎍/㎖ of each drug showed no recognizable cytotoxic effect, marked reductions of cell viability were detected at concentrations over 5.0㎍/㎖. [3H]thymidine incorporation assay for cell proliferation demonstrated that DNA replication of SK-MEL-2 cells is inhibited by Apamin and Phospholipase A2 in a dose-dependent manner. Consistent with this result, the cells were accumulated at the G1 phase of the cell cycle after treatment with Apamin and Phospholipase A2, whereas no detectable change in cell proliferation was identified by Melittin treatment. In addition, tryphan blue exclusion and flow cytometric analyses showed that all of these drugs can trigger apoptotic cell death of SK-MEL-2, suggesting that Melittin, Apamin, and Phospholipase A2 have antitumorigenic potential through the suppression of cell growth and/or induction of apoptosis. Qantitative RT-PCR analysis revealed that Apamin and Phospholipase A2 inhibit expression of growth-promoting genes such as c-Jun, c-Fos, and Cyciin D1. Furthermore, Phospholipase A2 induced tumor suppressors p53 and p21/Wafl. In addition, all three drugs were found to activate expression of a representative apoptosis-inducing gene Bax while expression of apoptosis-suppressing Bcl-2 and Bcl-XL genes was not changed. Taken together, this study strongly suggests that Metittin, Apamin, and Phosphalipase A2 may have antitumorigenic activities, which are associated with its growth-inhibiting and/or apoptosis-inducing potentials.

• Journal of Ginseng Research
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• v.23 no.3 s.55
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• pp.190-197
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• 1999

In this study, the molecular mechanism of the growth inhibitory effect of panaxynol was investigated in a human malignant melanoma cell line, SK-MEL-l. In the cell cycle analysis, panaxynol arrested cell cycle progression of SK-MEL-I at the G1 phase. Immunoblot analysis demonstrated that panaxynol increased $p21^{WAF1}$ and decreased cdc2 expression. Protein levels of pl6, p27, E2F-1, Rb, and p53 were not changed. Thus, the changes in expression levels of $p21^{WAF1}$ and cdc2 apparently mediate the cell cycle arrest caused by panaxynol. In addition, cycloheximide (CHX) partially reversed the growth inhibition by panaxynol, which suggested that new protein synthesis was required. On the other hand, LLnL, a proteasome inhibitor, increased antiproliferative effect of panaxynol. This may be due to stabilization of the protein(s) responsible for the growth inhibition such as $p21^{WAF1}$. In summary, these results demonstrate that panaxynol inhibits proliferation of SK-MEL-I by inducing cell cycle arrest at the G1 phase and the inhibitory effect is mediated by the increased level of $p21^{WAF1}$ as well as decreased cdc2 expression.