Betaine Protects Against Rotenone-Induced Neurotoxicity in PC12 Cells

Rotenone is an inhibitor of mitochondrial complex I-induced neurotoxicity in PC12 cells and has been widely studied to elucidate the pathogenesis of Parkinson’s disease. We investigated the neuroprotective effects of betaine on rotenone-induced neurotoxicity in PC12 cells. Betaine inhibited rotenone...

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Bibliographic Details
Published in:Cellular and molecular neurobiology 2013-07, Vol.33 (5), p.625-635
Main Authors: Im, A-Rang, Kim, Young-Hwa, Uddin, Md. Romij, Chae, Sungwook, Lee, Hye Won, Kim, Yun Hee, Kim, Yeong Shik, Lee, Mi-Young
Format: Article
Language:English
Subjects:
Animals
Betaine - pharmacology
Biomedical and Life Sciences
Biomedicine
Caspases - metabolism
Cell Biology
Energy Metabolism - drug effects
Enzyme Activation - drug effects
Flow Cytometry
In Situ Nick-End Labeling
Membrane Potential, Mitochondrial - drug effects
Microscopy, Confocal
Mitochondria - drug effects
Mitochondria - metabolism
Neurobiology
Neuroprotective Agents - pharmacology
Neurosciences
Neurotoxins - toxicity
Original Research
PC12 Cells
Rats
Rotenone - toxicity
Superoxides - metabolism
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Summary:Rotenone is an inhibitor of mitochondrial complex I-induced neurotoxicity in PC12 cells and has been widely studied to elucidate the pathogenesis of Parkinson’s disease. We investigated the neuroprotective effects of betaine on rotenone-induced neurotoxicity in PC12 cells. Betaine inhibited rotenone-induced apoptosis in a dose-dependent manner, with cell viability increasing from 50 % with rotenone treatment alone to 71 % with rotenone plus 100-μM betaine treatment. Flow cytometric analysis demonstrated cell death in the rotenone-treated cells to be over 50 %; the number of live cells increased with betaine pretreatment. Betaine pretreatment of PC12 cells attenuated rotenone-mediated mitochondrial dysfunction, including nuclear fragmentation, ATP depletion, mitochondrial membrane depolarization, caspase-3/7 activation, and reactive oxygen species production. Western blots demonstrated activation of caspase-3 and caspase-9, and their increased expression levels in rotenone-treated cells; betaine decreased caspase-3 and caspase-9 expression levels and suppressed their activation. Together, these results suggest that betaine may serve as a neuroprotective agent in the treatment of neurodegenerative diseases.
ISSN:0272-4340
1573-6830
1573-6830
DOI:10.1007/s10571-013-9921-z