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.