Abstract
Cimiside E was isolated from the Cimicifuga heracleifolia Komarov extract, which has been previously demonstrated to possess apoptotic action on gastric cancer cells. The IC(50) value of cimiside E on gastric cancer cells for 24 h was 14.58 microM. The mechanism of apoptosis was further elucidated through western blot, RT-PCR, morphology, Annexin V-FITC/PI staining and cell cycle analysis. Cell cycle arrest was induced by cimiside E in S phase at a lower concentration (30 microM) and G2/M phase at higher concentrations (60 and 90 microM). Cimiside E mediated apoptosis through the induction of the caspase cascade for both the extrinsic and intrinsic pathways. These findings suggest that cimiside E may be an effective chemopreventive agent against cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Annexin A5 / metabolism
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Antineoplastic Agents, Phytogenic / isolation & purification
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Antineoplastic Agents, Phytogenic / pharmacology*
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Apoptosis / drug effects*
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Blotting, Western
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Cell Cycle / drug effects*
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Cell Line, Tumor
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Cell Proliferation / drug effects
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Cimicifuga / chemistry*
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DNA Fragmentation / drug effects*
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Fas Ligand Protein / metabolism
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Humans
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Reverse Transcriptase Polymerase Chain Reaction
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Saponins / isolation & purification
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Saponins / pharmacology*
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Stomach Neoplasms / pathology*
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Triterpenes / isolation & purification
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Triterpenes / pharmacology*
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fas Receptor / metabolism
Substances
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Annexin A5
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Antineoplastic Agents, Phytogenic
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FAS protein, human
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FASLG protein, human
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Fas Ligand Protein
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Saponins
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Triterpenes
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cimiside E
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fas Receptor