2000PubMedRequires access

[The mechanisms of inhibitory effect of bufalin on human leukemia cells].

Rui‐Hua Xu, X Chen, L Chen, Jingyu Qian

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Abstract

OBJECTIVE: To study the mechanism of bufalin on human leukemia cell inhibition. METHODS: HL-60 cells were treated with bufalin at different concentrations. The growth inhibition was analysed by MTT assay, cell apoptosis by light microscopy, transmission electron microscopy, flow cytometry, TUNEL labeling method and agarose gel electrophoresis. RESULTS: (1) Treatment of HL-60 cells with bufalin remarkably inhibited the cell growth, the IC(50) value of bufalin for HL-60 cells was 0.025 micromol/L. (2) Apoptosis of HL-60 cells could be efficiently induced by bufalin at concentration of 0.010 micromol/L or higher. (3) Bufalin induced apoptosis of HL-60 cells in a dose- and time-dependent manner. (4) With G(1) phase cells decreasing, S phase cells increased, and then apoptotic cells increased with a diminution of S phase cells. (5) Bufalin-induced apoptosis of HL-60 cells was inhibited by ZnCl(2), an inhibitor of endonuclease, but not by cycloheximide, an inhibitor of protein synthesis. CONCLUSION: Bufalin could efficiently induce apoptosis of HL-60 cells, especially the S phase cells.

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What this paper is about

OBJECTIVE: To study the mechanism of bufalin on human leukemia cell inhibition. METHODS: HL-60 cells were treated with bufalin at different concentrations. The growth inhibition was analysed by MTT assay, cell apoptosis by light microscopy, transmission electron microscopy, flow cytometry, TUNEL labeling method and agarose gel electrophoresis. RESULTS: (1) Treatment of HL-60 cells with bufalin remarkably inhibited the cell growth, the IC(50) value of bufalin for HL-60 cells was 0.025 micromol/L. (2) Apoptosis of HL-60 cells could be efficiently induced by bufalin at concentration of 0.010 micromol/L or higher. (3) Bufalin induced apoptosis of HL-60 cells in a dose- and time-dependent manner. (4) With G(1) phase cells decreasing, S phase cells increased, and then apoptotic cells increased with a diminution of S phase cells. (5) Bufalin-induced apoptosis of HL-60 cells was inhibited by ZnCl(2), an inhibitor of endonuclease, but not by cycloheximide, an inhibitor of protein synthesis. CONCLUSION: Bufalin could efficiently induce apoptosis of HL-60 cells, especially the S phase cells.

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Available abstract

OBJECTIVE: To study the mechanism of bufalin on human leukemia cell inhibition. METHODS: HL-60 cells were treated with bufalin at different concentrations. The growth inhibition was analysed by MTT assay, cell apoptosis by light microscopy, transmission electron microscopy, flow cytometry, TUNEL labeling method and agarose gel electrophoresis. RESULTS: (1) Treatment of HL-60 cells with bufalin remarkably inhibited the cell growth, the IC(50) value of bufalin for HL-60 cells was 0.025 micromol/L. (2) Apoptosis of HL-60 cells could be efficiently induced by bufalin at concentration of 0.010 micromol/L or higher. (3) Bufalin induced apoptosis of HL-60 cells in a dose- and time-dependent manner. (4) With G(1) phase cells decreasing, S phase cells increased, and then apoptotic cells increased with a diminution of S phase cells. (5) Bufalin-induced apoptosis of HL-60 cells was inhibited by ZnCl(2), an inhibitor of endonuclease, but not by cycloheximide, an inhibitor of protein synthesis. CONCLUSION: Bufalin could efficiently induce apoptosis of HL-60 cells, especially the S phase cells.

Key concepts: Bufalin, Apoptosis, Chemistry, Flow cytometry, Cycloheximide, Molecular biology, Cell cycle, MTT assay

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