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.
Lu, T.-Y.; Kao, P.-F.; Lee, C.-M.; Huang, S.-T.; and Lin, C.-M.
"C 60 fullerene nanoparticle prevents β-amyloid peptide induced cytotoxicity in neuro 2A cells,"
Journal of Food and Drug Analysis: Vol. 19
, Article 17.
Available at: https://doi.org/10.38212/2224-6614.2263