C60 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 A beta-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 beta-amyloid (A beta)(25-35)-induced toxicity toward Neuro-2A cells in this study. PEG-C-60-3 reduced A beta(25-35)-induced cytotoxicity, which showed an increasing cell viability with C-60 and A beta(25-35) co-treated cells. Moreover, the intracellular reactive oxygen species (ROS) accumulation caused by A beta-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 A beta(25-35) treatment. The results offered new comprehension into the possible pathway of A beta(25-35) gene expression and C-60 protective mechanism. With the understanding of the roles of A beta and C-60 in cells, we can hopefully provide insight on therapeutic design using C-60 fullerene nanoparticles against A beta-associated diseases.