Journal
NEUROSCIENCE LETTERS
Volume 503, Issue 3, Pages 250-255Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.08.047
Keywords
Amyotrophic lateral sclerosis; Resveratrol; Nicotinamide; Sirtuin; Mitochondria biogenesis
Categories
Funding
- National Natural Sciences Foundation of China [81030019, 30871359]
- Beijing Natural Science Foundation [7082099, 7102161]
- Capital Medical Technology Development Foundation [SF-2009-III-34]
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Resveratrol has recently been widely reported to be an age-delaying and neuroprotective compound, and it appears to produce these benefits by activating silent mating type information regulation 2 homolog 1 (SIRT1). However, the role that SIRT1 activation plays in the pathogenesis of amyotrophic lateral sclerosis (ALS) remains unclear. In the present study. SIRT1 expression was found to be much lower in the mutant hSOD1G93A-bearing VSC4.1 cells compared to hSOD1wt cells when both were cultured in low-serum medium, indicating the involvement of SIRT1 activation defects in the pathogenesis of ALS under energetic stress. Further investigation revealed that a 24-h treatment with 0.5-20 mu M resveratrol had a dose-dependent protective effect on this ALS cell model, and the effects of resveratrol on increasing cell viability, preventing cell apoptosis and elevating cellular ATP levels through promoting mitochondria biogenesis were blocked by SIRT1 inhibition. This further demonstrated a role for SIRT1 activation in the protection of neuronal cells from degeneration. These findings suggest that resveratrol can protect the ALS cell model from mutant SOD1-mediated toxicity through up-regulating the expression of SIRT1, which represents a potential therapeutic target for preventing the motor neuron degeneration in ALS patients. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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