• Korean Journal of Pharmacognosy
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• v.34 no.3 s.134
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• pp.237-241
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• 2003

This study was carried out to test the growth inhibitory effects of sesamolin obtained from sesame seeds. Sesamolin inhibited the growth of human leukemia HL-60 cells in cultures and the synthesis of macromolecules in dose- and time-dependent manners. Sesamolin in the $60{\sims}100\;{\mu}g/ml$ range was cytostatic. At concentrations greater than $200\;{\mu}g/ml$ sesamolin was cytocidal to HL-60 cells and at $60\;{\mu}g/ml$ inhibited the synthesis of DNA, RNA and protein in HL-60 cells by 35.1, 6.1, and 5.3%, whereas at $200\;{\mu}g/ml$ these inhibitions were 86.8%, 81.5% and 96.7%, respectively. The inhibitory effect of sesamolin on DNA synthesis was irreversible.

• Archives of Pharmacal Research
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• v.25 no.4
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• pp.480-484
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• 2002

Costunolide has been reported to be a cytotoxic and chemopreventive agent. This work investigated the mechanism of the anti proliferative effect of costunolide and determined that it induced differentiation of the human leukemia cell line HL-60. Costunolide exhibited a potent antiproliferative activity against HL-60 cells. It was also found to be a potent inducer of differentiation in human leukemia derived HL-60 cells through the examination of differentiation markers, as assessed by the reduction of nitroblue tetrazolium, the increase in esterase activities and phagocytic activity, morphology change and the expression of CD14 and CD66b surface antigens. These results, accompanied by a decline in the expression of c-myc protein, suggest that costunolide induces differentiation of human leukemia cells to granulocytes and monocytes/macrophages lineage.

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 2004.06a
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• pp.297-301
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• 2004

The purpose of the present study was to investigate the anti-proliferative and apoptotic effects of MCS-C2, a novel analogue of toyocamycin and sangivamycin, in human promyelocytic leukemia (HL-60) cells. When treated with MCS-C2, inhibited proliferation associated with cell cycle arrest and apoptotic induction was found in the HL-60 cells in a concentration-dependent and time-dependent manner. This apoptotic induction was associated with the cleavage of Bid and a release of cytochrome c from mitochondria into the cytosol, followed by the activation of caspase-3 and inactivation of poly (ADP-ribose) polymerase (PARP). However, there was no significant change in any other mitochondrial membrane proteins, such as Bcl-2 and Bax. Consequently, the current findings suggest that the mitochondrial pathway was primarily involved in the MCS-C2-induced apoptosis in the human promyelocytic leukemia HL-60 cells.

• Journal of Nutrition and Health
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• v.36 no.4
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• pp.382-388
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• 2003

(-)-Epigallocatechin-3-gallate (EGCG) is a polyphenolic compound found in peen tea leaves, and has been known to be one of the most potent catechin species which inhibits cell growth most possibly through an apoptotic cell death. We investigated the apoptotic activity of (-)-EGCG on the human myeloid leukemia cell line, HL-60. Our results of MTT test indicated that (-)-EGCG had a significant antiproliferation effect in HL-60 cells with $IC_{50}$/ (50% inhibition concentration) value of 65 $\mu$M. Giemsa statining of HL-60 cells treated with (-)-EGCG (100 $\mu$M) for 6hrs showed a typical apoptosis-specific morphological change including shrinkage of the cytoplasm, membrane blobbing and compaction of the nuclear chromatin. The DNA fragmentation was observed from the agarose gel electrophoresis of cells treated with (-)-EGCG for 3hrs or longer, and was progressed to a greater degree as treatment time increases. Treatment of the cells with (-)-EGCG (100 $\mu$M) resulted in a rapid release of mitochondrial cytochrome c into the cytosol, and a subsequent cleavage of caspase-3 to an active form in a treatment-time dependent manner. (-)-EGCG (100 $\mu$M) also stimulated proteolytic cleavage of poly-(ADP-ribose) polymerase (PARP) to an active form in HL-60 cells. Tlken together, (-)-EGCG appears to induce the apoptosis in human myeloid leukemia cells via a caspase-dependent pathway. These results suggest the possible application of (-)-EGCG, the major active compound in green tea, as an antiproliferative agent for cancer prevention.

• YAKHAK HOEJI
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• v.47 no.5
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• pp.319-324
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• 2003

This study examined the inhibitory effect of extracts of Trichosanthes kirilpwii sorted according to the parts on the growth of HL-60 cells. The growth of HL-60 leukemia cells was markedly inhibited by the treatment of the 80％ methanol extract of roots (10 $\mu\textrm{g}$/mι), stems (50$\mu\textrm{g}$/mι), pips (10$\mu\textrm{g}$/mι), and gourds (100 $\mu\textrm{g}$/mι), or the ethylacetate fraction of leaves (100 $\mu\textrm{g}$/mι). when the HL-60 cells were treated with the extracts of T. kirilpwii sorted according to the parts, DNA fragmentation and sub-G1 hypodiploid cells were observed. Moreover, T. kirilpwii extracts increased the level of the expression of the active form of caspase-3 and the activation of caspase-3 was demonstrated by the cleavage of poly(ADP-ribose) polymerase, a vital substrate of effector caspase. The results suggest that the inhibitory effect of extracts of T. kirilpwii sorted according to the parts on the growth of HL-60 cells seems to arise from the induction of apoptosis.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.215.1-215.1
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• 2003

We investigated the in vitro effect of Acteoside , phenylpropanoid glycosides. is a natural product isolated from …. on proliferation, differentiation and cell cycle regulation in human promyelocytic HL -60 leukemia cells. Acteoside significantly inhibited the proliferation of HL -60 cells, with IC50 of about 30$\mu\textrm{g}$/$m\ell$. It was also found to be a potent inducer of differentiation in human leukemia derived HL-60 cells through the examination of differentiation markers. (omitted)

• YAKHAK HOEJI
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• v.45 no.2
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• pp.161-168
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• 2001

The possible mechanism of the antiproliferative and apoptotic effects of Boswellia carterri water extract were studied in HL-60 human leukemia cells. The cytotoxicity of HL-60 cells after the treatment of Boswellia carterii water extract showed dose- and time-dependent manner. The apoptotic effect of 300 $\mu$g/ml Boswellia carterii water extract was demonstrated by DNA laddering. The activity of caspase 3-1ike protease was markedly increased in HL-60 cells treated with Boswellia carterii water extract. Furthermore, the level of Bcl-2 was time-dependently reduced, whereas Bax protein level was enhanced by Boswellia carterii water extract treatment. In conclusion, our results suggest that apoptotic effect of Boswellia carterii water extract may partly mediated through activations of caspase-3 activity and Bax expression, and inhibition of Bcl-2 expression.

• BMB Reports
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• v.40 no.6
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• pp.1009-1015
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• 2007

In this communication, we report the efficacy of $\beta$-carotene towards differentiation and apoptosis of leukemia cells. Dose ($20{\mu}M$) and time dependence (12 h) tests of $\beta$-carotene showed a higher magnitude of decrease (significance p < 0.05) in cell numbers and cell viability in HL-60 cells than U937 cells but not normal cell like Peripheral blood mononuclear cell (PBMC). Microscopical observation of $\beta$-carotene treated cells showed a distinct pattern of morphological abnormalities with inclusion of apoptotic bodies in both leukemia cell lines. When cells were treated with $20{\mu}M$ of $\beta$-carotene, total genomic DNA showed a fragmentation pattern and this pattern was clear in HL-60 than U937 cells. Both the cell lines, on treatment with $\beta$-carotene, showed a clear shift in $G_1$ phase of the cell cycle. In addition the study also revealed anti-oxidant properties of $\beta$-carotene since there was reduction in relative fluorescent when treated than the control at lower concentration. Collectively this study shows the dual phenomenon of apoptosis and differentiation of leukemia cells on treatment with $\beta$-carotene.

• YAKHAK HOEJI
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• v.52 no.1
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• pp.1-6
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• 2008

The present study investigated the antiproliferative effects of Crnum asiaticum var. japonicum against HL-60 human leukemia cells. The 80% MeOH extract or several solvent fractions from the C. asiaticum inhibited the growth of HL-60 cells, whereas the growth of HEL-299 cells, human embryonic lung fibroblast, was scarcely inhibited. When the HL-60 cells were treated with the $CHCl_3$ fraction, the BuOH fraction, the EtOAc fraction and the $H_2O$ fraction, DNA ladder, chromatin condensation and increase of sub-G1 hypodiploid cells were observed. Furthermore, the $CHCl_3$ fraction and the BuOH fraction reduced Bc1-2 mRNA level, whereas Bax mRNA level was increased. These results suggest that the inhibitory effect of C. asiaticum on the growth of the HL-60 cell might be mediated through the induction of apoptosis via the down-regulation of Bc1-2. Taken together, components of C. asiaticum might have a therapeutic potential for the treatment of human leukemia.

• Archives of Pharmacal Research
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• v.19 no.2
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• pp.91-94
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• 1996

In the course of a search for antitumor agents, we found that the extract of Curcuma longa was effective in inducing apoptosis or programmed cell death (PCD) in human myeloid leukemia cells (HL-60). Active compounds for PCD were isolated from the hexanic extraction of the rhizome of Curcuma longa. With the several chromatographies, and spectral data, they were identified as ar-turmerone and $\beta-atlantone$. The present results demonstrate that the exposure of human myeloid leukemia HL-60 cells to clinically achievable concentrations of arturmerone (TU) or .$\beta-atlantone$(AT) produced internucleosomal DNA fragmentation of approximately 200 base-pair multiples, and the morphological changes characteristic of cells undergoing apoptosis or PCD. This findings suggest that these agents may exert their antitumoral activity, in part, through induction of apoptosis(PCD).