• Title/Summary/Keyword: Hacat cell

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Anti-cancer and anti-inflammatory effects of convergence of ginsenoside Rh2, compound K isolated from amplified red ginseng (증폭시킨 홍삼으로부터 분리한 ginsenoside Rh2, compound K의 융복합적 항암 및 항염효과)

  • Kim, Young-Ho;Kim, Jong-Du
    • 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.

Chemical Constituents of Silene seulensis Nakai from Demilitarized Zone(DMZ)

  • Jung, Yeon Woo;Seo, Chan Gon;Lee, Ji Eun;Hong, Seong Su;Kwon, Jin Gwan;Shin, Hyun Tak;Jung, Su Young;Choi, Jeong Jun;Choi, Chun Whan;Kim, Jin Kyu
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2018.10a
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    • pp.92-92
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    • 2018
  • Silene seulensis Nakai was used as traditional medicines in Korea, we collected plant from demilitarized zone (DMZ). S. seulensis was extracted with 30, 50, and 70% ethanol and partitioned successively with n-hexane, EtOAc, dichloromethane and BuOH. These extracts (30, 50 and 70% ethanol) were evaluated the cytotoxicity on B16F10 and Hacat cell lines. The LC-MS/MS data of each fractions (n-hexane, EtOAc, dichloromethane, and BuOH) were compared with MS library, combined with ultraviolet/visual (UV/Vis) and MS data for faster determine structure by database search results. This led to the identification of four compounds (1-4) from S. seulensis. These compounds was isolated first time from S. seulensis. Their chemical structures are elucidated by combinations of NMR and mass spectrometry techniques.

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The Effect of Propofol on Hypoxic damaged-HaCaT Cells

  • Park, Chang-Hoon;Kwak, Jin-Won;Park, Bong-Soo;Kim, Yong-Ho;Kim, Yong-Deok;Yoon, Ji-Uk;Yoon, Ji-Young;Kim, Cheul-Hong
    • Journal of The Korean Dental Society of Anesthesiology
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    • v.14 no.1
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    • pp.41-47
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    • 2014
  • Background: Autophagy is a self-eating process that is important for balancing sources of energy at critical times in development and in response stress. Autophagy also plays a protective role in removing clearing damaged intracellular organelles and aggregated proteins as well as eliminating intracellular pathogens. The purpose of the present study was to examine the protective effect of propofol against hypoxic damage using keratinocytes. Methods: Human keratinocytes (HaCaT cells) were obtained from the American Type Culture Collection. Propofol which were made by dissolving them in DMSO were kept frozen at $-4^{\circ}C$ until use. The stock was diluted to their concentration with DMEM when needed. Prior to propofol treatment cells were grown to about 80% confluence and then exposed to propofol at different concentrations (0, 25, 50, 75, $100{\mu}M$) for 2 h pretreatment. Cell viability was measured using a quantitative colorimetric assay with thiazolyl blue tetrazolium bromide (MTT assay), and fluorescence microscopy and western blot analysis were used for evaluation of autophagy processes. Results: The viability of propofol-treated HaCaT cells was increased in a dose-dependent manner. Propofol did not show any significant toxic effect on the HaCaT cells. The autophagy inhibitor, 3-methyladenine, reduced cell viability of hypoxia-injured HaCat cells. Fluorescence microscopy and western blot analysis showed propofol induce autophagy pathway signals. Conclusions: Propofol enhanced viability of hypoxia-injured HaCaT cells and we suggest propofol has cellular protective effects by autophagy signal pathway activation.