Abstract
We used a rat pheochromocytoma (PC12) cell line to study the effects of salidroside on hydrogen peroxide (H(2)O(2))-induced apoptosis. In PC12 cells, H(2)O(2)-induced apoptosis was accompanied by the down-regulation of Bcl-2, the up-regulation of Bax, the release of mitochondrial cytochrome c to cytosol, and the activation of caspase-3, -8 and -9. However, salidroside suppressed the down-regulation of Bcl-2, the up-regulation of Bax and the release of mitochondrial cytochrome c to cytosol. Moreover, salidroside attenuated caspase-3, -8 and -9 activation, and eventually protected cells against H(2)O(2)-induced apoptosis. Taken together, these results suggest that treatment of PC12 cells with salidroside can block H(2)O(2)-induced apoptosis by regulating Bcl-2 family members and by suppressing cytochrome c release and caspase cascade activation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects*
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Bisbenzimidazole / metabolism
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Caspases / analysis
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Caspases / metabolism*
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Cell Survival / drug effects
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Cytochromes c / metabolism*
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DNA Fragmentation
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Dose-Response Relationship, Drug
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Drugs, Chinese Herbal / pharmacology
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Enzyme Activation / drug effects
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Fluorescent Dyes / metabolism
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Formazans / analysis
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Formazans / metabolism
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Glucosides / pharmacology*
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Hydrogen Peroxide / toxicity
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L-Lactate Dehydrogenase / analysis
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L-Lactate Dehydrogenase / metabolism
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PC12 Cells
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Phenols / pharmacology*
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Protective Agents / pharmacology*
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RNA, Messenger / metabolism
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Rats
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Tetrazolium Salts / analysis
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Tetrazolium Salts / metabolism
Substances
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Drugs, Chinese Herbal
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Fluorescent Dyes
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Formazans
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Glucosides
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Phenols
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Protective Agents
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RNA, Messenger
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Tetrazolium Salts
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MTT formazan
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Cytochromes c
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Hydrogen Peroxide
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L-Lactate Dehydrogenase
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Caspases
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Bisbenzimidazole
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rhodioloside