• Title/Summary/Keyword: Apoptosis induction

Search Result 1,114, Processing Time 0.046 seconds

Effect of Butanol Fraction of Mylabris phalerata on Induction of Apoptosis in U937 cells (반묘 BuOH층의 U937 세포주에 대한 apoptosis유도 효과)

  • 허정은;윤택준;이종수;정진홍;김성훈
    • YAKHAK HOEJI
    • /
    • v.45 no.5
    • /
    • pp.484-490
    • /
    • 2001
  • Mylabris phalerata(MP) is an insect that has been used for the treatment of cancer in oriental medicine. To evaluate the anticancer activity of Mylabris phalerata, We measured the cytotoxicity of Mylabris phalerata solvent fractions such as MC, EA, BuOH and residual layers on U937, human monocytic leukemia cells. Of those fractions BuOH layer of Mylabris phalerata was the most effective with ID$_{50}$ of 140$\mu\textrm{g}$/ml. It effectively caused DNA fragmentation from the concentration of 50$\mu\textrm{g}$/ml, showed apoptotic nucleus by tenets assay and expressed apototic portion stained by Annexin-V. It also induced the activation of caspase-3 and cleavage of the substrate poly (ADP-ribose) polymerase (PARP). These results suggest BuOH layer of Mylabris phalerata exerts anticancer activity by induction of apoptosis via activation of caspase-3 protease.e.

  • PDF

Tributyltin Induce Apoptosis by Induction of Nur 77 Expression and Translocation in to the Cytosol in Leydig Cells

  • Park, Chul-Yung;Lee, Kyung-Jin;Kim, Ji-Young;Oh, Duk-Hee;Shin, Dong-Weon;Jung, Kyung-Sik;Jeong, Hye-Gwang
    • Proceedings of the Korean Society of Toxicology Conference
    • /
    • 2003.10b
    • /
    • pp.138-138
    • /
    • 2003
  • Tributyltin (TBT) is also recognized as an endocrine disrupter. Organotin compounds such as TBT are widely used as agricultural biocides, and for antifouling paint of ship bottoms and of fishing nets. In this study, we investigated the role of nur 77 in induction of apoptosis in TBT-induced leydig cells.(omitted)

  • PDF

Induction of apoptosis in human promyelocytic leukaemia HL -60 cells by yomogin involves release of cytochrome c and activation of caspase

  • Jeong, Seoung-Hee;Koo, Sung-Ja;Ryu, Shi-Yong;Park, Hee-Jun;Lee, Kyung-Tae
    • Proceedings of the PSK Conference
    • /
    • 2002.10a
    • /
    • pp.319.1-319.1
    • /
    • 2002
  • Yomogin. an eudesmane sesquiterpene isolated from Artemisia princeps, was found to induce apoptosis in human promyelocytic leukaemia, HL -60 cell with characteristic apoptotic features like nuclear condensation, apoptotic body formation, flipping of membrane phosphatidylserine, release of mitochondrial cytochrome c and caspase-8. -9. and -3 activation. Furthermore. early yomogin-induced cytochrome c release was not affected by the caspase inhibitor Z-VAd fmk and preceded loss of mitochondrial membrane potential. The results suggest that induction of apoptosis by yomogin may provide a pivotal mechanism for their cancer chemopreventive function.

  • PDF

Apoptosis Induction of Persicae Semen Extract in Human Promyelocytic Leukemia (HL-60) Cells

  • Kwon, Hee-Young;Hong, Seon-Pyo;Hahn, Dong-Hoon;Kim, Jeong-Hee
    • Archives of Pharmacal Research
    • /
    • v.26 no.2
    • /
    • pp.157-161
    • /
    • 2003
  • The major ingredient of Persicae Semen is a cynogenic compound, amygdalin (D-mandelonitrile-$\beta$-gentiobioside). Controversial results on the anticancer activity of amygdalin were reported due to its conversion to its inactive isomer, neoamygdalin. In order to inhibit the epimerization of amygdalin, we used newly developed simple acid boiling method in preparation of Persicae Semen extract. HPLC analysis revealed most of amygdalin in Persicae Semen extract was active D-form. Persicae Semen extract was used to analyze its effect on cell proliferation and induction of apoptosis in human promyelocytic leukemia (HL-60) cells. Persicae Semen extract was cytotoxic to HL-60 cells with $IC_{50}$ of 6.4 mg/mL in the presence of 250 nM of $\beta$-glucosidase. The antiproliferative effects of Persicae Semen extract appear to be attributable to its induction of apoptotic cell death, as Persicae Semen extract induced nuclear morphology changes and internucleosomal DNA fragmentation.

Apoptosis Induction Effect of Zingiberis Rhizoma Extract in Microglia BV-2 Cells

  • Seo, Jeongbin;Oh, Myung Sook;Jang, Young Pyo;Kim, Jeong Hee
    • International Journal of Oral Biology
    • /
    • v.42 no.1
    • /
    • pp.9-15
    • /
    • 2017
  • Microglia have multiple functions in regulating homeostasis of the central nervous system. Microglia cells have been implicated as active contributors to neuron damage in neurodegenerative disorders. In this study, medicinal plant extracts (MPEs) were used to evaluate the cell-death induction effect in microglia BV-2 cells. Among 35 MPEs tested in this study, 4 MPEs showed less than a 30% cell survival after 24 hours of incubation. These were Foeniculi Fructus, Forsythiae Fructus, Zingiberis Rhizoma and Hedera Rhombea. The concentration showed that 50% cell death ($IC_{50}$) occurred with 33, 83, 67 Ed highlight: Please confirm wording, and $81{\mu}/ml$, respectively. For further study, we chose Zingiberis Rhizoma (ZR) which showed a reasonably low $IC_{50}$ value and an induction of cell death in a relatively narrow range. Western blot analysis showed that ZR-treated cells showed activation of caspase-3 and cleavage of PARP Ed highlight: When an acronym is first presented it needs to be spelled out in both dose- and time-dependent manners. However, the level of Bcl-2 and Bax were not changed by ZR-treatment in BV-2 cells. These results suggest that ZR-induced apoptosis in BV-2 cells occured through caspase-3 activation. The results also suggested that ZR may be useful in developing treatments for neurodegenerative diseases.

Induction of Apoptosis by Baicalein in Human Leukemia HL-60 Cells

  • Kim, Jang-Ho;Park, Sun-Young;Shin, Kwang-Sig;Yoo, Byung-Sun
    • Toxicological Research
    • /
    • v.17 no.2
    • /
    • pp.131-137
    • /
    • 2001
  • Baicalein, a major flavonoid of extract from Scutellaria baicalensis Georgi, has been shown to exhibit antioxidant and anti proliferative effects. In the present study, we investigate the effects of baicalein on viability and induction of apoptosis in human promyelocytic leukemia HL-60 cells. Baicalein was found to induce apoptosis of HL-60 cells in a concentration-dependent and time-dependent manner. When HL-60 cells were exposed to 100 $\mu\textrm{M}$ baicalein for 6h, the viability was decreased remarkably to 27% of control, whereas DNA fragmentation was significantly increased to 64%. Nucleosomal fragmentation of baicalein treated HL-60 cells, a hallmark of apoptosis, was further identified by agarose gel electrophoresis (DNA ladder). Flow cytometric analysis showed that apoptotic cells were increased to 66.6% after treatment with 100 $\mu\textrm{M}$ baicalein for 6 h. Baicalein-induced apoptosis of HL-60 cells was reduced by 1h pretreatment with inhibitor of caspases, z-Asp-$CH_2$-DCB. At 3 and 10 $\mu\textrm{M}$ of z-Asp-$CH_2$-DCB, DNA fragmentation of HL-60 cells induced by baicalein (50 $\mu\textrm{M}$) was 36.8 and 17.1 %, respectively, whereas, that of HL-60 cells treated by baicalein (50 $\mu\textrm{M}$) without pretreatment with inhibitor of caspases was 62.7%. These data suggest that baicalein induces apoptosis in human leukemia HL-60 cells, and that caspase enzymes might be involved in baicalein-induced apoptosis.

  • PDF

Effects of polysaccharides derived from Orostachys japonicus on induction of cell cycle arrest and apoptotic cell death in human colon cancer cells

  • Ryu, Deok-Seon;Baek, Geum-Ok;Kim, Eun-Young;Kim, Ki-Hoon;Lee, Dong-Seok
    • BMB Reports
    • /
    • v.43 no.11
    • /
    • pp.750-755
    • /
    • 2010
  • Crude Orostachys japonicus polysaccharide extract (OJP) was prepared by hot steam extraction. Polysaccharides (OJPI) were separated from OJP by gel filtration chromatography and phenol-sulfuric acid assay. The average molecular weight of the OJPI was 30-50 kDa. The anti-proliferative effect of OJPI on HT-29 human colon cancer cells was investigated via morphology study, cell viability assay, apoptosis assay, cell cycle analysis, and cDNA microarray. OJPI inhibited proliferation and growth of HT29 cells and also stimulated apoptosis in a dose- and time-dependent manner. In cell cycle analysis, treatment with OJPI resulted in a marked increase of cells in the G0 (sub G1) and G2/M phases. To screen for genes involved in the induction of cell cycle arrest and apoptosis, the gene expression profiles of HT-29 cells treated with OJPI were examined by cDNA microarray, revealing that a number of genes were up- or down-regulated by OJPI. Whereas several genes involved in anti-apoptosis, cell proliferation and growth, and cell cycle regulation were down-regulated, expression levels of several genes involved in apoptosis, tumor suppression, and other signal transduction events were up-regulated. These results suggest that OJPI inhibits the growth of HT-29 human colon cancer cells by various apoptosis-aiding activities as well as apoptosis itself. Therefore, OJPI deserve further development as an effective agent exhibiting anticancer activity.

Cobrotoxin Inhibits Prostate Carcinoma PC-3 Cell Growth Through Induction of Apoptotic Cell Death Via Inactivation of NF-kB

  • Song, Kyung-Chul;Song, Ho-Sueb
    • Journal of Acupuncture Research
    • /
    • v.23 no.2
    • /
    • pp.47-59
    • /
    • 2006
  • We previously found that cobrotoxin inhibited $NF-{\kappa}B$ activity by reacting with signal molecules of $NF-{\kappa}B$ which is critical contributor in cancer cell growth by induction of apoptotic cell death. We here investigated whether cobrotoxin inhibits cell growth of human prostate cancer cells through induction of apoptotic cell death, which is related with the suppression of the $NF-{\kappa}B$ activity. Cobrotoxin $(0{\sim}8\;nM)$ inhibited prostate cancer cell growth through increased apoptosis in a dose dependent manner. Cobrotoxin inhibited DNA binding activity of $NF-{\kappa}B$, an anti-apoptotic transcriptional factor. Consistent with the induction of apoptosis and inhibition of $NF-{\kappa}B$, cobrotoxin increased the expression of pro-apoptotic proteins caspase 3. Cobrotoxin, a venom of Vipera lebetina turanica, is a group of basicpeptides composed of 233 amino acids with six disulfide bonds formed by twelve cysteins. NF-kB is activated by subsequent release of inhibitory IkB and translocation of p50. Since sulfhydryl group is present in kinase domain of p50 subunit of NF-kB, cobrotoxin could modify NF-kB activity by protein-protein interaction. And Cobrotoxin down regulated Akt signals. Salicylic acid as a reducing agent of Sulf-hydryl group and LY294002 as a Akt inhibitor abrogated cobrotoxin-induced cell growth and DNA binding activity of $NF-{\kappa}B$. These findings suggest that nano to pico molar range of cobrotoxin could inhibit prostate cancer cell growth, and the effect may be related with the induction of apoptotic cell death through Akt dependent inhibition of $NF-{\kappa}B$ signal.

  • PDF

Mechanism of FHIT-Induced Apoptosis in Lung Cancer Cell Lines (폐암 세포주에서 FHIT 유전자 이입에 의한 Apoptosis의 기전)

  • Yoo, Jung Sun;Kim, Cheol Hyeon
    • Tuberculosis and Respiratory Diseases
    • /
    • v.56 no.5
    • /
    • pp.450-464
    • /
    • 2004
  • Background : The FHIT (fragile histidine triad) gene is a frequent target of deletions associated with abnormal RNA and protein expression in lung cancer. Previous studies have shown FHIT gene transfer into lung cancer cell line lacking FHIT protein expression resulted in inhibition of tumor cell growth attributable to the induction of apoptosis and reversion of tumorigenecity. However, the mechanism of the tumor suppressor activity of the FHIT gene and the cellular pathways associated with its function are not completely understood. Methods : To gain insight into the biological function of FHIT, we compared the NCI-H358 cell line with its stable FHIT transfectants after treatment with cisplatin or paclitaxel. We investigated the effects of FHIT gene expression on cell proliferation, apoptosis, and activation of caspase system and Bcl-2 family. The induction of apoptosis was evaluated by using DAPI staining and flow cytometry. Activation of caspases and Bcl-2 members was evaluated by Western blot analysis. Results : A significantly increased cell death was observed in FHIT transfectants after cisplatin or paclitaxel treatment and this was attributable to the induction of apoptosis. Remarkable changes in caspases and Bcl-2 family were observed in the transfected cells as compared with the control cells after treatment with paclitaxel. Activation of caspase-3 and caspase-7 was markedly increased in cells expressing FHIT. Expression level of Bcl-2 and Bcl-xL protein was significantly decreased and that of Bax and Bad protein was significantly increased in the transfected cells. Conclusion : FHIT gene delivery into lung cancer cells results in enhanced apoptosis induced by treatment with cisplatin or paclitaxel. The data suggest that apoptosis in FHIT-expressing cells could be related to activation of caspase pathway and Bcl-2 family.

Induction of Apoptotic Cell Death by Aqueous Extract of Cordyceps militaris Through Activation of Caspase-3 in Human Hepatocarcinoma Hep3B Cells (Hep3B 간암세포에서 Caspase-3 활성화를 통한 동충하초 열수추출물의 Apoptosis 유도에 관한 연구)

  • Kim, Kyung-Mi;Park, Cheol;Seo, Sang-Ho;Hong, Sang-Hoon;Lee, Won-Ho;Choi, Yung-Hyun
    • Journal of the Korean Society of Food Science and Nutrition
    • /
    • v.37 no.6
    • /
    • pp.714-720
    • /
    • 2008
  • Cordyceps militaris is a medicinal fungus which has been used for patient suffering from cancer in Oriental medicine. It was previously reported that C. militaris extracts are capable of inhibiting tumor growth and inducing apoptosis; however, the anti-poliferative effects of human cancer cells have been poorly understood. In this study, to elucidate the anti-cancer mechanisms of human cancer cells by treatment with aqueous extract of C. militaris (AECM), we investigated the anti-proliferative effects of AECM in human hepatocarcinoma Hep3B cells. AECM treatment inhibited the growth of Hep3B cells and induced the apoptotic cell death in a concentration-dependent manner such as formation of apoptotic bodies and increased populations of apoptotic-sub G1 phase. The induction of apoptosis by AECM was connected with a proteolytic activation of caspase-3 and caspase-8. and concomitant degradation of poly (ADP-ribose) polymerase (PARP) and ${\beta}$-catenin proteins. Furthermore, caspase-3 inhibitor, z-DEVD-fmk, significantly inhibited AECM-induced apoptosis demonstrating the important role of caspase-3 in the bserved cytotoxic effect. Taken together, these findings suggest that AECM-induced inhibition of human hepatocarcinoma cell proliferation is associated with the induction of apoptotic cell death via activation of caspase-3 and C. militaris may have therapeutic potential in human cancer.