Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 337, Issue 1-2, Pages 39-51Publisher
SPRINGER
DOI: 10.1007/s11010-009-0284-1
Keywords
Alzheimer's disease; Amyloid beta; Chitosan; NF-kappa B; Nrf2; NT2 neurons
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Funding
- National elite fund, Iran
- Young Scientist Research Fellowship
- Shahid Beheshti University
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Increased oxidative stress is a widely accepted factor in the development and progression of Alzheimer's disease. Here, we introduce chitosan, an antioxidant oligosaccharide, as a protective agent against H2O2/FeSO4-induced cell death in the NT2 neural cell line. Chitosan not only protects the neurons against cell death, as measured by MTT and caspase-3 activity, but also decreases amyloid beta formation. NT2 neurons can be used to elucidate the relationship between oxidative stress and A beta formation. We induced A beta formation through oxidative stress in NT2 neurons and studied the effect of chitosan. We demonstrate that chitosan can be neuroprotective by suppressing A beta formation. We further show that chitosan exerts its protective effect by up-regulation of HO-1, gamma-GCS, Hsp-70, and Nrf2, while it inhibits activation of caspase-3 and NF-kappa B. Chitosan or chitosan derivatives have potential value as neuroprotective agents, particularly with regard to oxidative stress.
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