Article Title

C 60 fullerene nanoparticle prevents β-amyloid peptide induced cytotoxicity in neuro 2A cells


Oxidative stress, which is an early determinant of Alzheimer's disease (AD), is involved in mediating neuronal apoptosis in Aβ-induced cell death. C 60 fullerenes are known to behave like a "radical sponge" as they can sponge up free radicals and act more effectively than other antioxidants. PEG-C 60-3, a C 60 fullerene derivative, was investigated against β-amyloid (Aβ) 25-35-induced toxicity toward Neuro-2A cells in this study. PEG-C 60-3 reduced Aβ 25-35-induced cytotoxicity, which showed an increasing cell viability with C 60 and Aβ 25-35 co-treated cells. Moreover, the intracellular reactive oxygen species (ROS) accumulation caused by Aβ-treated Neuro-2A cells was reduced by PEG-C 60-3 co-treatment. Microarray for the analysis of gene expressions was investigated. Endoplasmic reticulum (ER) stress responsive genes, ion-channel, cell-cycle and anti-oxidant related cell responses were found to be associated with C 60 protective mechanism against Aβ 25-35 treatment. The results offered new comprehension into the possible pathway of Aβ 25-35 gene expression and C 60 protective mechanism. With the understanding of the roles of Aβ and C 60 in cells, we can hopefully provide insight on therapeutic design using C 60 fullerene nanoparticles against Aβ-associated diseases.

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