Article

Molecular and Cellular Biochemistry

, Volume 337, Issue 1, pp 39-51

Chitosan prevents oxidative stress-induced amyloid β formation and cytotoxicity in NT2 neurons: involvement of transcription factors Nrf2 and NF-κB

  • Fariba KhodagholiAffiliated withNeuroscience Research Center, Shahid Beheshti University of Medical Science Email author 
  • , Bahareh EftekharzadehAffiliated withNeuroscience Research Center, Shahid Beheshti University of Medical Science
  • , Nader MaghsoudiAffiliated withNeuroscience Research Center, Shahid Beheshti University of Medical Science
  • , Parisa Fathi RezaeiAffiliated withNeuroscience Research Center, Shahid Beheshti University of Medical Science

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Abstract

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 β formation. NT2 neurons can be used to elucidate the relationship between oxidative stress and Aβ formation. We induced Aβ formation through oxidative stress in NT2 neurons and studied the effect of chitosan. We demonstrate that chitosan can be neuroprotective by suppressing Aβ formation. We further show that chitosan exerts its protective effect by up-regulation of HO-1, γ-GCS, Hsp-70, and Nrf2, while it inhibits activation of caspase-3 and NF-κB. Chitosan or chitosan derivatives have potential value as neuroprotective agents, particularly with regard to oxidative stress.

Keywords

Alzheimer’s disease Amyloid beta Chitosan NF-κB Nrf2 NT2 neurons