• Korean Journal of Agricultural Science
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• v.40 no.4
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• pp.353-358
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• 2013

To demonstrate that follistatin treatment enhances the efficiency of nuclear transfer (SCNT), cell allocation and preimplantational development were determined in bovine SCNT embryos in the present study. Treatment of activated SCNT embryos with 10 ng/ml follistatin significantly increased the proportion of blastocyst development compared to untreated SCNT embryos. In addition, an increase in trophectoderm (TE) cell numbers and relatively higher proportion of TE cells to total cells were observed, but the number of inner cell mass (ICM) cell and total cell numbers were not changed (P < 0.05). No significant effect of other doses of follistatin was observed for the above endpoints. However, treatment with 1 and 10 ng/ml follistatin reduced the proportion of nuclear transfer blastocysts with an ICM ratio of > 60% relative to untreated nuclear transfer blastocysts at Day 7. No significant effect of follistatin treatment on proportions of nuclear transfer blastocysts with ICM ratio of 20-40% or 40-60% was observed. Taken together, these results suggested that follistatin can be used to increase developmental competence of SCNT embryos in terms of cell allocation, particularly TE cells, during preimplantation stages, subsequently enhancing placentation and birth of live offspring.

• Journal of Sasang Constitutional Medicine
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• v.12 no.2
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• pp.171-183
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• 2000

1. Back ground and purpose An experimental study has done to examine the effect of defense and cure gastric mucasal damage of Mokdan-pijihwang-tang. 2. Methods Mice had intragastric injected with MJ extract before indomethacin treatment which induces homorrhage infarct and erosion artificially. Degree of lipid peroxidation, general morphology, change of mucous cell, the distribution of PNA, ICAM and distribution of apoptotic cell were objected. (Abbreviation) MJ : Mokdanpijihwang-tang, PNA : Peanut Agglutinin, ICAM : Intercellular Adhesion Molecule 3 Results 1) The degree of lipid peroxidation in INDO-group had increased conspicuously than control group. But the degree of lipid peroxidation in MJ-group had decreased than INDO-group and these decline had probability. 2) After indomethacin treatment, hemorrhage infarct and erosion had increased in stomach body. But in MJ-group, the configuration is normal, except the group intragastric injected with MJ extract at hour 24 before indomethacin treatment. 3) Surface mucous cell and neck mucous had disappeared in INDO-group. But in MJ-group tormal distribution had shown like control group except the group intragastric injected with MJ extract at hour 24 before indomethacin treatment. 4) PNA positive reaction had not shown in INDO-group. But medium PNA positive reaction had shown In Mj-group. 5) ICAM positive reacted cell had shown in INDO-group. The decrease of ICAM positive cell were shown than INDO-group. 6) A number of apoptotic cell was distributed in hemorrhagic erosion. A few number of apoptotic cell was distributed in MJ-group except some surface mucous. 4. Conclusion These results suggest that MJ has an effect on cure of gastric mucosal damage.

• YAKHAK HOEJI
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• v.51 no.3
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• pp.214-218
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• 2007

In the previous reports, we developed the CO5 by introducing genes for the first and second urea cycle enzymes, carbamoyl phosphate synthetase I (CPS I) and ornithine transcarbamoylase (OTC) into the IBE cell lines producing erythropoietin (EPO). The CO5 have been found out to have 15-20% higher cell growth rate and produce 2-times more EPO than the parental cell line, IBE. To investigate the role of CPS I in CO5 cell line for the cell growth and amount of EPO, we knock-downed CPS I gene expression via siRNA treatment. Expression level of EPO in cell lysate of CO5 was 3-5 fold higher than that of IBE. After siRNA treatment, the cell growth of CO5 was decreased 8-21% and the EPO productivity in the cell Iysate was significantly decreased. However, these changes of the cell growth and EPO productivity were not observed in IBE. These results indicate that CPS I gene expression is important for the increased cell growth and EPO productivity of CO5 cell line.

• International Journal of Contents
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• v.8 no.4
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• pp.74-77
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• 2012

Radiation has been an effective tool for treating cancer for a long time. Radiation therapy induces DNA damage within cancer cells and destroys their ability to reproduce. Radiation therapy is often combined with other treatments, like surgery and chemotherapy. Here, we describe the effects of radiation and histone deacetylase inhibitor, Trichostain A, on cell cycle regulation in hepatoma cells. The combinatorial treatment of radiation and Trichostain A induced cell cycle arrest and thereby increasing the hepatoma cell death. Furthermore, the regulatory effects of radiation and Trichostatin A on cell cycle applied in cell type specifically. These results suggest that the treatment of radiation and Trichostatin A may play a central role in hepatoma cell death and might be a good remedy to improve the efficiency of radiation therapy.

• Journal of Pharmacopuncture
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• v.18 no.2
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• pp.26-32
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• 2015

Objectives: Rheum undulatum L. has traditionally been used for the treatment of many diseases in Asia. However, its anti-proliferative activity in cancer has still not been studied. In the present study, we investigated the anti-cancer effects of methanol extract of Rheum undulatum L. (MERL) on human adenocarcinoma gastric cell lines (AGS). Methods: To investigate the anti-cancer effect of MERL on AGS cells, we treated the AGS cells with varying concentrations of MERL and performed 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays. Cell cycle analyses, measurements of the mitochondrial membrane potential (MMP), caspase activity assays and Western blots were conducted to determine whether AGS cell death occurred by apoptosis. Results: Treatment with MERL significantly inhibited growth of AGS cells in a concentration dependent manner. MERL treatment in AGS cells leaded to increased accumulation of apoptotic sub G1 phase cells in a concentration dependent manner. In control cultures, 5.38% of the cells were in the sub G1 phase. In MERL treated cells, however, this percentage was significantly increased (9.95% at $70{\mu}g/mL$, 15.94% at $140{\mu}g/mL$, 26.56% at $210{\mu}g/mL$ and 38.08% at $280{\mu}g/mL$). MERL treatment induced the decreased expression of pro-caspase-8 and -9 in a concentration dependent manner, whereas the expression of the active form of caspase-3 was increased. A subsequent Western blot analysis revealed increased cleaved levels of poly (ADP-ribose) polymerase (PARP) protein. Also, treatment with MERL increased the activities of caspase-3 and -9 compared with the control. MERL treatment increased the levels of the pro-apoptotic truncated Bid (tBid) and Bcl2 Antagonist X (Bax) proteins and decreased the levels of the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein, whose is the stabilization of mitochondria. However, inhibitions of p38, extracellular signal regulated kinases (ERKs) and C-Jun N-terminal kinases (JNK) by MERL treatment did not affect cell death. Conclusion: These results suggest that MERL mediated cell death is associated with an intrinsic apoptotic pathway in AGS cells.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.194-198
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• 2013

Recent papers have shown that the initial event in the pathogenesis of autoimmune type 1 diabetes (T1D) comprises sensing of molecular patterns released from apoptotic ${\beta}$-cells by innate immune receptors such as toll-like receptor (TLR). We have reported that apoptotic ${\beta}$-cells undergoing secondary necrosis called 'late apoptotic' ${\beta}$-cells stimulate dendritic cells (DCs) and induce diabetogenic T cell priming through TLR2. The role of other innate immune receptors such as TLR7 or TLR9 in the initiation of T1D has also been suggested. We hypothesized that TLR2 blockade could inhibit T1D at the initial step of T1D. Indeed, when a TLR2 agonist, $Pam3CSK_4$ was administered chronically, the development of T1D in nonobese diabetic (NOD) mice was inhibited. Diabetogenic T cell priming by DCs was attenuated by chronic treatment with $Pam3CSK_4$, indicating DC tolerance. For the treatment of established T1D, immune tolerance alone is not enough because ${\beta}$-cell mass is critically reduced. We employed TLR2 tolerance in conjunction with islet transplantation, which led to reversal of newly established T1D. Dipeptidyl peptidase 4 (DPP4) inhibitors are a new class of anti-diabetic agents that have beneficial effects on ${\beta}$-cells. We investigated whether a combination of DPP4 inhibition and TLR2 tolerization could reverse newly established T1D without islet transplantation. We could achieve normoglycemia by TLR2 tolerization in combination with DPP4 inhibition but not by TLR2 tolerization or DPP4 inhibition alone. ${\beta}$-cell mass was significantly increased by combined treatment with TLR2 tolerization and DPP4 inhibition. These results suggest the possibility that a novel strategy of TLR tolerization will be available for the inhibition or treatment of established T1D when combined with measures increasing critically reduced ${\beta}$-cell mass of T1D patients such as DPP4 inhibition or stem cell technology.

• Journal of Periodontal and Implant Science
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• v.38 no.4
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• pp.595-602
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• 2008

Purpose: Ti-6Al-4V alloy is widely used as an implant material because of its good biocompatibility and good mechanical property compared with commercial pure titanium. Otherwise, toxicity of aluminum and vanadium in vivo has been reported. Ti-8Ta-3Nb alloy is recently developed in the R&D Center for Ti and Special Alloys and it was reported that this alloy has high mechanical strength, no cytotoxicity and similar biocompatibility to commercial pure titanium, but many studies are needed for its clinical use. In these experiment, we carried out different surface treatment on each Ti-8Ta-3Nb alloy disks, then cultured cell on it and assessed biological response. Materials and Methods: cpTi, Ti-6Al-4V, Ti-8Ta-3Nb alloy disks were prepared and carried out sandblasting and acid etching (SLA) or alkali-heat treatment (AH) on the Ti-8Ta-3Nb alloy disks. We cultured primary rat calvarial cells on each surface and assessed early cell attachment and proliferation by scanning electron microscopy, cell proliferation, alkaline phosphatase activity. Result: The rates of cell proliferation on the cpTi, Ti-8Ta-3Nb AH disks were higher than others (p<0.05) and alkaline phosphatase activity was significantly enhanced on the Ti-STa-8Nb AH disks(p<0.05). Conclusion: Most favorable cell response was shown on the Ti-8Ta-3Nb AH surfaces. It is supposed that alkali-heat treatment of the Ti-8Ta-3Nb alloy could be induced earlier bone healing and osseointegration than smooth surface.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.23
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• pp.10085-10089
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• 2015

Background: The insulin-like growth factor (IGF) system comprises a group of proteins that play key roles in regulating cell growth, differentiation, and apoptosis in a variety of cellular systems. The aim of this study was to investigate the role of insulin-like growth factor binding protein 3 (IGFBP3) in hepatocellular carcinoma. Materials and Methods: Expression of IGF2, IGFBP3, and PTEN was analyzed by qRT-PCR. Lentivirus vectors were used to overexpress IGFBP3 in hepatocellular carcinoma cell (HCC) lines. The effect of IGFBP3 on proliferation was investigated by MTT and colony formation assays. Results: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells. Conclusions: Expression of IGF2, IGFBP3, and PTEN in several HCC cell lines was lower than in normal cell lines. After 5-aza-2'-deoxycytidine/trichostatin A treatment, significant demethylation of the promoter region of IGFBP3 was observed in HCC cells. Overexpression of IGFBP3 induced apoptosis and reduced colony formation in HUH7 cells.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.46 no.6
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• pp.682-688
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• 2013

In this study, we investigated about cell toxicity and oxidative stress of HepG2 cell by treatment of sodium fluoride (NaF) and fluoride extracts from krill Euphausia superba meat, shell, whole body and krill meal. The cell toxicity showed significant at 300 and $500{\mu}g/mL$ NaF treatment group. But krill (Euphausia superba) fluoride extract (KFE) treatment in all groups were not toxic. The superoxide radical production increased significantly in NaF treated group, but there was no significant change in KFE treated group. The superoxide dismutase activity was a significant increase 21.5% at $100{\mu}g/mL$ and 24.7% at $300{\mu}g/mL$ treatment group of fluoride extracts from krill meat, and 8.7% at $300{\mu}g/mL$ in krill meals, compared to the control group. However, hydroxy radical flux and catalase and glutathione peroxidase activity of fluoride extracts from krill meat did not change. As a result, for a short period of time, NaF treatment in HepG2 cells affect the cell toxicity and oxidative stress, but in the case of KFE, these were not recognized. Thus, depending on the type of food ingested with fluoride, cell toxicity and oxidative stress was found to be different.

• Molecules and Cells
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• v.42 no.12
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• pp.884-892
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• 2019

Piperlongumine (PL), a natural alkaloid compound isolated from long pepper (Piper longum), can selectively kill cancer cells, but not normal cells, by accumulation of reactive oxygen species (ROS). The objective of this study was to investigate functional roles of expression of SETDB1 and FosB during PL treatment in MCF7 breast cancer cells. PL downregulates SETDB1 expression, and decreased SETDB1 expression enhanced caspase 9 dependent-PARP cleavage during PL-induced cell death. PL treatment generated ROS. ROS inhibitor NAC (N-acetyl cysteine) recovered SETDB1 expression decreased by PL. Decreased SETDB1 expression induced transcriptional activity of FosB during PL treatment. PARP cleavage and positive annexin V level were increased during PL treatment with FosB overexpression whereas PARP cleavage and positive annexin V level were decreased during PL treatment with siFosB transfection, implying that FosB might be a pro-apoptotic protein for induction of cell death in PL-treated MCF7 breast cancer cells. PL induced cell death in A549 lung cancer cells, but molecular changes involved in the induction of these cell deaths might be different. These results suggest that SETDB1 mediated FosB expression may induce cell death in PL-treated MCF7 breast cancer cells.