• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.6
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• pp.1383-1392
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• 2003

Apoptosis is a morphologically and biochemically district form of cell death that occurs in many different cell types in a wide variety of organisms. Albizzia julibrissin belonging the family Leguminosae has been used for the treatment of contusion, sore throat, amnesia, and insomnia in oriental traditional medicine. This study investigates whether the water extract of A. julibrissin induce apoptotic cell death in Jurkat T-acute lymphoblastic leukemia (ALL) cells. Jurkat cells were increased inhibitions of cell viability in a concentration-dependent manner by A. julibrissin. This herbal medicine also caused apoptosis as measured by cell morphology and DNA fragmentation. The capability of A. julibrissin to induce apoptosis was associated with proteolytic cleavage of specific target proteins such as poly (ADP-ribose)polymerase (PARP) and beta-catenin proteins suggesting the possible involvement of caspases. Our result showed that Bcl-2 and Bax protein levels were not changed in all A. julibrissin-treated groups compared to control group. These results suggest that A. julibrissin-mediated apoptosis is independent with Bcl-2 related signaling pathway in this cells. The purpose of the present study is also to investigate the Effect of A. julibrissin on cell cycle progression. Our results showed that G1 checkpoint related gene products (cyclin D1, cyclin dependent kinase 4, retinoblastoma, E2F1) were decreased in their protein levels in a dose-dependent manners after treatment of the extract. These results indicate that the increase of apoptotic cell death by A. julibrissin may be due to the inhibition of cell cycle progression in wild type p53-lacking Jurkat cells.

• Journal of Life Science
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• v.19 no.5
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• pp.676-679
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• 2009

In order to produce a new antibiotic material against Jurkat T cells using horizontal gene transfer among microbes, co-cultures between soil bacteria AY2000 and the multiple antibiotic producer S. griseus was carried out. It showed that the highest active substance against Jurkat T cells was produced at 48 hr of co-culture time with MTT assay. Moreover, a morphological change of nuclear of Jurkat T cells treated with co-cultured substance was observed in DAPI staining. This result suggests that a new material was produced with co-culture supernatant, and that co-culture between microboes can develop new antibiotic materials.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.2
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• pp.338-345
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• 2003

The purpose of this research was to investigate the anticancer effects of Dojeokseungki-tang(DJSKT) on the various leukemia cell lines. DJSKT treatment suppressed proliferation of cultured-HL60, Jurkat, L1210 cells and increased apoptosis of cultured-L1210, HL60, Molt4, Jurkat cells. DJSKT treatment induced apoptosis of Jurkat cells including the morphologic changes such as the 'ladder pattern' revealed by agarose gel electrophoresis of DNA in a dose-dependent manner. Administration of DJSKT induced apoptosis of transplanted-L1210 cells in vivo, and decreased of mitochondrial transmembrane potential of L 1210 and Jurkat cells in vitro. DJSKT treatment reduced the expression of bcl-2 proteins in Jurkat cells and increased ICE, c-myc, p53 mRNA expression in Molt4 cells. In conclusion, these results suggest that DJSKT might be usefully applied for anti-carcinogenic agent of leukemia.

• Journal of Life Science
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• v.11 no.1
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• pp.8-18
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• 2001

The purpose of this study was to evaluate the genotypic characterization of Actinobacillus actinomycetemcomitans (A. actinomycetemcomitans) using arbitrarily primed polymerase chain reaction (AP-PCR), to investigate the cytotoxicity of both clinical isolates and standard strains of A. actinomycetemcomitans for the human Jurkat T cells, and to measure the osteoclastogenic cytokines released by Jurkat cells infected with these bacterial strains. The random sequence primer 15 and 16 could distinguish different AP-PCR profiles between clinical isolates of A. actinomycetemcomitans. A. actinomycetemcomitans significantly suppressed Jurkat cell viability in time dependent fashion and the results of DNA fragmentation assay indicated that this bacterial species induced apoptosis in Jurkat cells undergoing apoptosis released the osteoclastogenic cytokine, IL-1$\beta$, IL-6, TNF-$\alpha$. These data support the hypothesis that induction of apoptosis is at least one essential step in A. actinomycetemcomitans induced local immunosuppressive pathway, and that A. actinomycetemcomitans can modulate the immunomodulatory cell population in the periodontal tissue by inducing T cell death through apoptosis, and that apoptosis of local resident T cells may play an active role in bone resorption by releasing osteoclastogenic cytokines, e.g. IL-1$\beta$, IL-6, TNF-$\alpha$.

• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.3
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• pp.372-378
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• 2011

We extracted polysaccharide from the sea hare, Aplysia kurodai, purified it partially, and experimented its immune response using the human blood lymphocytes and macrophage cell lines. Aplysia kurodai polysaccharide fraction (APF) improved the growth of the T cell (Jurkat) up to 40% by treatment for 48 hours, and decreased the growth of blood cancer, Jiyoye cell line. The APF on RAW 264.7 cell also increased interleukin-12 up to 47%. In contrast, the secretion of interleukin-2 and interferon-gamma by treatment of only APF or APF and concanavalin A on Jurkat for 24 hours and 48 hours didn't influence significantly. These results suggest that the APF has possible immune regulating ability.

• Korean Journal of Pharmacognosy
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• v.39 no.2
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• pp.150-154
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• 2008

Butein is a one of polyphenolic compound widely available in numerous plants. It has broad biological activities including antioxidant and anti-inflammatory activities, which contributed to its protective effects against cancer. Evidences that butein influence proliferation of tumor cells make it important to determine how butein affects cell death of various cancers. In this study, we show that butein, a phenolic compound, induces apoptosis in human T lymphoma jurkat cells. We found that treatment of cells with butein increased apoptosis in a dose- and time- dependent manner as determined by staining cells with Annexin V and 7AAD. There was no significant apoptotic cell death when normal lymphocytes and monocytes from healthy donor were treated with butein. We also found caspase-3 activity was increased during butein-induced apoptosis. The buteininduced apoptotic cell death was blocked by the treatment of cells with caspase-3 inhibitor. These results indicate that butein has the potential to provide an effective strategy against cancer with the advantage of being widely avalible.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.6
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• pp.1190-1196
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• 2002

Selaginella Tamariscina is widely used in the traditional oriental herbal medicine for its anti-inflammatory, anti-cancer effects. The effects of aqueous extracts of Selaginella Tamariscina (ST) on the cell viability and induction of apoptotic cell death were investigated in A549, Raw 264.7, C6-glioma. Jurkat and HL-60 cells. The cell viability after treating with extract of Selaginella Tamariscina was quantified by MTT assay method. The results showed that ST decreased the cell viability in HL-60 and Jurkat cells not in A549, Raw 264.7 and C6-glioma cells. And we also observed the chromatin condensation and DNA fragmentation in HL-60 and Jurkat cells. The enzyme activity of caspase-3, tightly regulated by an apoptosis activating complex, were markedly increased in HL-60 cells treated with the ST by dose-dependent manner. In conclusion, our results suggest that the extract of Selaginella Tamariscina may induce the selective apoptotic cell death in HL-60 and Jurkat cells via activation of caspase-3.

• Molecular & Cellular Toxicology
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• v.1 no.2
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• pp.116-123
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• 2005

The application of high pressure on cellular morphology, proliferation and protein expression of Jurkat cells (human T lymphocyte cell line) has been extensively investigated. In the present study, we manufactured a novel pressure chamber that modulates 5% $CO_{2}$, temperature and pressure (up to 3 ATA). Jurkat cells was incubated 2 ATA pressure and analyzed cellular morphology and growth using an electron microscopy and MTT assay. The cells showed the morphological changes in the cell surface, which appeared to cause a severe damage in cell membrane. The growth rate of the cells under 2 ATA pressure decreased as cultured time got increased. Furthermore, a long term exposure of high pressure on Jurkat cells may act as one of the important cellular stresses that leads to inducing cell death. Cellular proteomes were separated by 2-dimensional electrophoresis with pH 3-10 ranges of IPG Dry strips. And many proteins showed significant up-and-down expressions with hyperbaric pressure. Out of all, 10 spots were identified significantly using matrix-assisted laser desorption/ionization-time of fight (MALDI-TOF) mass spectrometry. We and found that 9 protein expressions were decreased and one protein, heat shock protein HSP 60, was increased in Jurkat cells under 2 ATA. Identified proteins were related to lipid metabolism and signal transduction.

• Journal of Life Science
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• v.13 no.1
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• pp.118-127
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• 2003

$\rho$-Fluorophenylalanine (FPA), a phenylalanine analog, is able to induce apoptotic cell death of human acute leukemia Jurkat T cells. To better understand the mechanism by which FPA induces apoptotic cell death, the effect of ectopic expression of antiapoptotic proteins, Bcl-2 and Bcl-xL, on FPA-induced apoptosis was investigated by employing lurkat T cells transfected with Bcl-2 gene (JT/Bcl-2) or Bcl-xL gene (1/Bcl-xL) and Jurkat T cells transfected with vector (JT/Neo or J/Neo). When Jurkat T cells, JT/Neo or J/Neo, were exposed to FPA at concentrations ranging from 0.63 to 5.0 mM, the cell viability determined by MTT assay declined in a dose-dependent manner. In addition, apoptotic DNA fragmentation along with several apoptotic events such as caspase-8 activation, Bid cleavage, mitochondrial cytochrome c release, caspase-9 activation, caspase-3 activation, and degradation of PARP was induced. However, the FPA-induced cytotoxic effect, activation of caspase-8, and cleavage of Bid were significantly abrogated by ectopic expression of Bcl-2 or Bcl-xL. At the same time, there was marked reduction in the level of cytochrome c release from mitorhondria, caspase-9 activation, caspase-3 activation, and degradation of PARP. These results indicate that caspase-8 activation, Bid cleavage, and mitochondrial cytochrome c release with subsequent activation of the caspase cascade are negatively regulated by Bcl-2 or Bcl-xL, and are thus required for FPA-induced apoptosis in Jurkat T cells

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.1
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• pp.73-78
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• 2014

Cell death and survival are tightly controlled through the highly coordinated activation/inhibition of diverse signal transduction pathways to insure normal development and physiology. Imbalance between cell death and survival often leads to autoimmune diseases and cancer. Death receptors sense extracellular signals to induce caspase-mediated apoptosis. Acting upstream of CED-3 family proteases, such as caspase-3, Bcl-2 prevents apoptosis. Using short hairpin RNAs (shRNAs), we suppressed Bcl-2 expression in Jurkat T cells, and this increased TCR-triggered AICD and enhanced TNFR gene expression. Also, knockdown of Bcl-2 in Jurkat T cells suppressed the gene expression of FLIP, TNF receptor-associated factors 3 (TRAF3) and TRAF4. Furthermore, suppressed Bcl-2 expression increased caspase-3 and diminished nuclear factor kappa B (NF-${\kappa}B$) translocation.