Abstract
Allicin, the main flavor compound in garlic, has anti-carcinogenic activities in a range of cancer cells, however, the underlying molecular mechanisms are not completely understood. This study examined the effect of allicin on the cell viability of U87MG human glioma cells along with its molecular mechanisms of induction of cell death. Apoptosis was determined by TUNEL and Hoechst 33258 staining as well as by western blot analysis. Allicin inhibited the cell viability of U87MG human glioma cells in a dose- and time-dependent manner. Allicin-induced inhibition of cell viability was due to apoptosis of cells. The mechanisms of apoptosis were found to involve the mitochondrial pathway of Bcl-2/Bax, the MAPK/ERK signaling pathway and antioxidant enzyme systems. These results suggest that allicin can serve as a novel chemotherapeutic candidate for the treatment of glioblastoma multiforme.
MeSH terms
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Acetylcysteine / pharmacology
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Antineoplastic Agents / pharmacology*
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Antioxidants / pharmacology
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Apoptosis / drug effects*
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Butadienes / pharmacology
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Caspases / metabolism
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Catalase / pharmacology
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Cell Line, Tumor
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Cell Proliferation / drug effects*
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Cell Shape / drug effects
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Cell Survival / drug effects
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Disulfides
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Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors
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Extracellular Signal-Regulated MAP Kinases / metabolism*
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Glioblastoma
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Humans
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Imidazoles / pharmacology
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MAP Kinase Signaling System / drug effects
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Nitriles / pharmacology
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Phosphorylation
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Pyridines / pharmacology
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Sulfinic Acids / pharmacology*
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bcl-2-Associated X Protein / metabolism
Substances
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Antineoplastic Agents
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Antioxidants
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BAX protein, human
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Butadienes
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Disulfides
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Imidazoles
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Nitriles
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Proto-Oncogene Proteins c-bcl-2
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Pyridines
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Sulfinic Acids
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U 0126
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bcl-2-Associated X Protein
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allicin
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Catalase
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Extracellular Signal-Regulated MAP Kinases
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Caspases
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SB 203580
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Acetylcysteine