Abstract
Ciprofloxacin (CPFX) and roxithromycin (RXM) induced apoptosis of activated Jurkat T cells in vitro. CPFX showed concentration-dependent acceleration of apoptosis of activated Jurkat T cells by enhancing the expression of FasL and activities of caspase-3 and -8. RXM accelerated cell death, enhanced expression of FasL and caspase-3 but not caspase-8, and did not show the concentration dependency.
MeSH terms
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Anti-Bacterial Agents / pharmacology*
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Anti-Infective Agents / pharmacology*
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Apoptosis / drug effects*
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Caspases / biosynthesis
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Cell Survival / drug effects
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Ciprofloxacin / pharmacology*
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DNA Fragmentation
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Enzyme-Linked Immunosorbent Assay
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Fas Ligand Protein
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Fluorescein-5-isothiocyanate
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Fluorescent Antibody Technique
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Genes, bcl-2 / genetics
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Humans
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Jurkat Cells
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Membrane Glycoproteins / biosynthesis
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Proto-Oncogene Proteins / genetics
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Proto-Oncogene Proteins c-bcl-2*
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Roxithromycin / pharmacology*
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T-Lymphocytes / drug effects*
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T-Lymphocytes / metabolism
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bcl-2-Associated X Protein
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fas Receptor / biosynthesis
Substances
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Anti-Bacterial Agents
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Anti-Infective Agents
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FASLG protein, human
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Fas Ligand Protein
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Membrane Glycoproteins
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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bcl-2-Associated X Protein
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fas Receptor
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Roxithromycin
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Ciprofloxacin
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Caspases
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Fluorescein-5-isothiocyanate