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Betaine Protects Against Rotenone-Induced Neurotoxicity in PC12 Cells
Cited 31 time in
Web of Science
Cited 33 time in Scopus
- Authors
- Issue Date
- 2013-07
- Publisher
- SPRINGER/PLENUM PUBLISHERS
- Citation
- CELLULAR AND MOLECULAR NEUROBIOLOGY, Vol.33 No.5, pp.625-635
- Keywords
- PARKINSONS-DISEASE ; DEATH ; MECHANISMS ; CASPASE-3 ; NUTRITION ; MODELS ; RATS
- Abstract
- 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-mu M 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
- Language
- English
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