Quercetin induced apoptosis in human leukemia HL-60 cells. 1997

D Xiao, and S P Zhu, and Z L Gu
Department of Pharmacology, Suzhou Medical College, China.

OBJECTIVE To examine whether quercetin (Que) might induce apoptosis in human leukemia HL-60 cells. METHODS DNA fragmentation was visualized by agarose gel electrophoresis. Inhibition of proliferation was measured with a colorimetric MTT-assay. The DNA degradation was determined using flow cytometry, and the microscopic changes were observed by an electron microscope. RESULTS Que 15-120 mumol.L-1 elicited typical apoptosis morphological changes including condensed chromatin, nuclear fragmentation, and reduction in volume. DNA fragmentation and DNA degradation in a concentration-dependent manner in HL-60 cells. Que inhibited HL-60 cell proliferation. The values of IC50 and 95% confidence limits were 43 (30-61) mumol.L-1 after 48-h treatment with Que. CONCLUSIONS Que induced apoptosis in HL-60 cells.

UI MeSH Term Description Entries
D011794 Quercetin A flavonol widely distributed in plants. It is an antioxidant, like many other phenolic heterocyclic compounds. Glycosylated forms include RUTIN and quercetrin. 3,3',4',5,7-Pentahydroxyflavone,Dikvertin
D002455 Cell Division The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION. M Phase,Cell Division Phase,Cell Divisions,Division Phase, Cell,Division, Cell,Divisions, Cell,M Phases,Phase, Cell Division,Phase, M,Phases, M
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000972 Antineoplastic Agents, Phytogenic Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity. Antineoplastics, Botanical,Antineoplastics, Phytogenic,Agents, Phytogenic Antineoplastic,Botanical Antineoplastics,Phytogenic Antineoplastic Agents,Phytogenic Antineoplastics
D017209 Apoptosis A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis
D053938 DNA Fragmentation Splitting the DNA into shorter pieces by endonucleolytic DNA CLEAVAGE at multiple sites. It includes the internucleosomal DNA fragmentation, which along with chromatin condensation, are considered to be the hallmarks of APOPTOSIS. DNA Degradation, Apoptotic,Apoptotic DNA Degradation,Fragmentation, DNA
D018922 HL-60 Cells A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8) HL60 Cells,Cell, HL60,Cells, HL60,HL 60 Cells,HL-60 Cell,HL60 Cell

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