• Title/Summary/Keyword: Apotosis

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Effect of Aralia Cordata Pharmacopuncture on Cartilage Protection and Apoptosis Inhibition In Vitro and in Collagenased-induced Arthritis Rabbit Model

  • Park, Dong-Suk;Baek, Yong-Hyeon
    • The Journal of Korean Medicine
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    • v.28 no.4
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    • pp.114-123
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    • 2007
  • Osteoarthritis is characterized by cartilage degradation and chondrocytes death. Chondrocyte death is induced by the apotosis through special mechanisms including the activation of caspase-3. On the basis of this background, this study was designed to examine the cartilage protective and anti-apototic effects of Aralia Cordata in in vtro and in collagenase-induced arthritis rabbit model. To conduct in vitro study, chondrocytes culturedfrom rabbit knee joint were treated by 5 ng/ml IL-1a.For in vivo experiment, collagenase-induced arthritis (CIA) rabbit model was made via intraarticular injection with 0.25 ml of collagenase solution. Aralia cordata pharmacopuncture (ACP) was administrated on bilateral Dokbi acupoint (ST35) of rabbits at a dosage of 150 ${\mu}g/kg$ once a day for 28 days after the initiation of the CIA induction. In the study by using CIA rabbit model in vivo, ACP showed the inhibition of cartilage degradation in histological analysis. Aralia cordata also showed anti-apoptotic effect both in vitro and in vivo study. In chondrocytes treated by IL-1a, Aralia cordata inhibited caspase-3 activity and enhanced the proliferation of IL-1a-induced dedifferentiated chondrocytes. ACP showed the inhibition effect on the caspase-3 expression and activity from CIA rabbit model. This study indicates that ACP inhibits the cartilage destruction and the chondrocyte apotosis through downregulation of caspase-3 activity. These data suggest that ACP has a beneficial effect on preventing articular cartilage destruction in osteoarthrtis.

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The Effect of Conjugated Linoleic Acid Isomers on the Cell Proliferation, Apotosis and Expressions of Uncoupling Protein (Ucp) Genes during Differentiation of 3T3-L1 Preadipocytes (Conjugated Linoleic Acid 이성체가 3T3-L1 지방전구세포 분화중 세포증식, 세포사멸 및 Ucp 유전자 발현에 미치는 영향)

  • Kwon So-Young;Kang Keum-Jee
    • Journal of Nutrition and Health
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    • v.37 no.7
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    • pp.533-539
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    • 2004
  • It has been reported that CLA decreases fat deposition in vivo and in vitro experiments. Among CLA isomers, c9t11 and t10c12 have been shown to exert active biological activities. For example, t10c12 reduces body weight and increases lean body mass, whereas, c9t11 has little effect on body fattness. However, the underlying molecular mechanism for the anti-obesity action of CLA isomers are not well understood. The purpose of this study was to examine the effects of t10c12 and c9t11 on lipid accumulation, cell proliferation, cell death and the expression levels of Ucp genes which are proposed as targets for anti-obesity in 3T3-L1 preadipocytes. Isomers of CLA at 50$\mu$M were added into preadipocyte differentiation medium for 3, 6 and 9days. Control cells received only the vehicle in the differentiation medium. Cytochemical analyses for lipid accumulation, cell proliferation and apotosis were carried out to compare lipidogenesis and cellular activity. RT-PCR analysis of GAPDH, Ucp 2,3 and 4 were also performed to find any modulatory effects of CLA isomers on the metabolic genes. Lipid accumulation indicated by Oil Red-O staining was inhibited in CLA isomers as compared to the control. T10c12 isomer showed less lipidogenesis than c9t11 did. A decrease occurred in CLA isomers as shown by BrdU incorporation. Apotosis has occured at higher level in t10c12 when compared to that of t9c11. Ucp 2, 3 and 4 genes were also upregulated in CLA isomers. T10c12 showed higher level of Ucp gene expressions than the c9t11 did. The biological activities of CLA isomers were also found to be different during differentiation of 3T3-L1 preadipocytes, suggesting that different isomers may be active in certain stage of lipidogenesis. The results indicate that both c9t11 and t10c12 CLA isomers decrease lipidogenesis, inhibit cell proliferation, increase cell death and upregulate in Ucp gene expressions during 3T3-L1 preadipocyte differentiation. T10c12 isomer was more effective than c9t11 in overall anti-obesity activity.

Induction of Apoptosis by Ginsenoside Rc on SK-MEL-28 Cell Lines (인체 흑색종세포에서 Ginsenoside Rc에 의한 Apoptosis의 유도)

  • Choi Su La;Myung Pyung Keun;Jeong Seung Il;Chun Hyun Ja;Baek Seung Hwa
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.17 no.1
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    • pp.209-212
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    • 2003
  • A wide variety of cancer chemotherapeutic agents have been shown to induce programmed cell death (PCD, apoptosis) in various tumor cell fines in vitro. This study was performed to know how ginsenoside Rc affect on SK-MEL-28 cell line, and how they induce the apoptosis. SK-MEL-28 cell lines were treated with various concentrations of ginsenoside Rc and cultured for various times. At cell cycle analysis, cells arrested at G2/M phase by ginsenoside Rc and apotosis percentage increased along with increasing concentration and time. TUNEL assay was performed to know whether SK-MEL-28 cell fine die as apoptosis or necrosis by ginsenoside Rc. As a result, fluorescence increased along with increasing time and concentration. Fas expressed on SK-MEL-28 cell lines membrane by ginsenoside Rc was identified using flow cytometer. Ginsenoside Rc induced apoptosis against SK-MEL-28 cell fines, and the apoptosis mechanism was identified as Fas-mediated apotosis.

Effect of Cyclin D2 on Cell Proliferation in T-47D Breast Cancer Cells (인체 유방암 세포에서 과다발현 시킨 Cyclin D2의 영향에 대한 연구)

  • 김현준;이근수;전상학;공구
    • Environmental Mutagens and Carcinogens
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    • v.24 no.1
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    • pp.1-9
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    • 2004
  • Three D-type cyelins (D1, D2, and D3) are expressed in G1 phase of the cell cyele and have been implicated in cell transformation and neoplasia in human and mouse. Cyclin D1 overexpression or amplification was described in various human cancers. However, there is controversy about the role of cyclin D2 in cell cyele progression and human carcinogenesis. Specially, loss of cyelin D2 is involved in a vital tumor suppressor function in normal breast tissue, and that its loss may be related to tumorigenesis. The author examined to effect over-expression of cyclin D2 on the cell proliferation, apoptosis, and cell cycle using cyclin D2 transfected stable T47D breast cancer cells to investigate whether cyclinD2 functions as a positive regulator or negative regulator in cell proliferation. Overexpression of cyclin D2 led to the suppression of cell growth in cyclin D2 transfected T47D in both in its expression level and a time dependent manner with up to 50% reduction of cell growth at 72 hours. Therefore, the authors performed the cell cycle phase analysis using the flow cytometry to investigate the effect of cyclin D2 on the cell cycle phase in cyclin D2 transfected stable T47D cells. The flow cytometry analysis revealed increased sub G0 phase in cyclin D2 transfeted cells up to 23% at 72 hours. To confirm these results induced by overexpression of cyclinD2, the apoptotic bodies were counted in control and cyclin D2 transfected T47 cells. There are markedly increases of apoptotic bodies in cyclin D2-transfected cells up to 18%. These results suggested that Cyclin D2 suppresses the cell proliferation in breast cancers cells via the induction of apotosis.

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Ethanolic Extract from Derris scandens Benth Mediates Radiosensitzation via Two Distinct Modes of Cell Death in Human Colon Cancer HT-29 Cells

  • Hematulin, Arunee;Ingkaninan, Kornkanok;Limpeanchob, Nanteetip;Sagan, Daniel
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.4
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    • pp.1871-1877
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    • 2014
  • Enhancing of radioresponsiveness of tumors by using radiosensitizers is a promising approach to increase the efficacy of radiation therapy. Recently, the ethanolic extract of the medicinal plant, Derris scandens Benth has been identified as a potent radiosensitizer of human colon cancer HT29 cells. However, cell death mechanisms underlying radiosensitization activity of D scandens extract have not been identified. Here, we show that treatment of HT-29 cells with D scandens extract in combination with gamma irradiation synergistically sensitizes HT-29 cells to cell lethality by apoptosis and mitotic catastrophe. Furthermore, the extract was found to decrease Erk1/2 activation. These findings suggest that D scandens extract mediates radiosensitization via at least two distinct modes of cell death and silences pro-survival signaling in HT-29 cells.

Mechanical/Biochemical Analysis of Cell Adhesion Strengthening (세포흡착 거동의 기계적/생화학적 분석)

  • Shin, Heung-Soo
    • Proceedings of the KSME Conference
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    • 2008.11a
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    • pp.1455-1457
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    • 2008
  • Cell adhesion is a coordinated process involving initial binding of integrin receptors to extracellular matrix (ECM), recruitment of adhesion proteins, and focal adhesion assembly. The formation of mechanically stable focal adhesion assembly of cells within surrounding ECM is a key parameter to direct numerous cellular functions including cell migration, differentiation, and apotosis. With current cell adhesion assays, it is difficult to understand contributions of each coordinated event on evolution of cell adhesion strengthening since cells spontaneously spread upon their adhesion to the substrate, thus remodeling their cytoskeletal structure. In this presentation, novel approaches for analysis of cell adhesion strengthening process based on the combination of mechanical device, micro-patterned substrates, and molecular biological techniques will be discussed.

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Optimazation of the Assement and Apotosis of Endocrine-Bisphenol A Disruptors (내분비계장애물질 평가방법의 최적화 및 Apoptosis에 관한 연구)

  • Ahn Kwang-Hyun;Lee Kyung-A;Kim Bong-Hee
    • Environmental Analysis Health and Toxicology
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    • v.19 no.3
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    • pp.251-259
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    • 2004
  • Xenoestrogens are chemicals with diverse structure that mimic estrogen. Bisphenol A, a monomer of polycarbonate and epoxy resins, has been detected in canned food and human saliva. Bisphenol A stimulate cell proliferation and induce expression of estrogen -response genes in vitro. The purpose of the this study was to evaluate cell proliferation of bisphenol A in the presence of a rat liver 59 mix contaning cytochrome P450 enzymes and Cu (II). The fragmentation of intact DNA, a parameter of apoptotic cell death, was evaluated quantitatively by diphenylamine reaction method. Bisphenol A induced apoptotic cell death in a dose-dependent manner The effect of radical scavenger on the apoptotic cell death induced bisphenol A was investigated. The DNA fragmentation induced by bisphenol A was significantly inhibited by addition of radical scavenger to the culture medium. This indicated that elevated oxidative stress caused by imbalance between the production and removal of free radicals occurred in cells. Taken together, these results suggest that free radical reacts with Cu (II) leading oxidative stress.

Effects of Ketamine and Pentobarbitone on Degeneration of Oocyte and Apoptosis of Granulosa Cells in Mouse Ovary (Ketamine과 Pentobarbitone이 생쥐 난자의 퇴화 및 과립세포의 자연세포사에 미치는 영향)

  • Kim, Jong-Hoon;Yoon, Yong-Dal
    • Clinical and Experimental Reproductive Medicine
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    • v.25 no.2
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    • pp.179-187
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    • 1998
  • In mammal, lots of follicles start simultaneously their growth but only a few oocytes are ovulated in every sexual cycles. Most of matured and grown oocytes are destined to degenerate by atresia. However, the molecular and physiological mechanisms are not elucidated yet. The present study was designed to establish an induction method of follicular atresia with ketamine or pentobarbitone and evaluate the effect of these anesthetics on oocyte maturation and granulosa cell apoptosis of the mouse ovarian follicle. The percentages of degenerated oocyte and apoptotic granulosa cell in ketamine treated groups were significantly higher than that in controls (58.9% vs 33.5%, p<0.01, degeneration; 44.9% vs 26.6%, p<0.01, apotosis). Futhermore, it was revealed that the concentrations of progesterone in both groups were markedly higher than that in control. In cunclusion, it is considered that ketamine induce an atresia as pentobarbitone, and may be useful for inducing follicular atresia.

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Apoptotic effect of formaldehyde in cultured human hepatocyte cell lines (인간 간세포주 에서 포름알데히드에 의한 세포 사멸 효과)

  • Park, Soo-Hyun
    • Korean Journal of Environmental Agriculture
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    • v.28 no.4
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    • pp.462-467
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    • 2009
  • Exposure of formaldehyde (FA), one of the major compounds in pesticides and in the onset of sick house syndrome, has been implicated in the development of diverse diseases. Liver is a very important organ to body metabolism and drug detoxification. Apotosis of hepatocytes is associated with the onset of liver diseases such as hepatitis. However, the apoptotic effect of FA in hepatocytes is not clear. Therefore, this study was conducted to investigate the effect of FA on the apoptosis in HepG2 cells, a human hepatocyte cell line. As a result, FA (> $500\;{\mu}M$) decreased cell viability and increased lactate dehydrogenase activity in HepG2 cells, which was blocked by the treatment of vitamin E and N-acetylcysteine (NAC). In addition, FA decreased glutathione (GSH) contents and Bcl-2 levels, while increasing lipid peroxide formation and Bax levels. It also cleaved caspase-3 form, which was blocked by the treatment of vitamin E and NAC. It is insisted that FA induced apoptosis via oxidative stress in human hepatocytes.