C60 Fullerene Nanoparticle Prevents β-Amyloid Peptide Induced Cytotoxicity in Neuro 2A Cells
TAN-YI LU1#, PAI-FENG KAO1,2#, CHI-MING LEE3, SHENG-TUNG HUANG4 AND CHUN-MAO LIN1*
1. School of Medicine, Taipei Medical University, Taipei, Taiwan, R.O.C.
2. Division of Cardiology, Wan Fang Hospital, Taipei, Taiwan, R.O.C.
3. Core Facility Center, Taipei Medical University, Taipei, Taiwan, R.O.C.
4. Institute of Biotechnology, National Taipei University of Technology, Taipei, Taiwan, R.O.C.
(Received: December 9, 2010; Accepted: April 7, 2011)
ABSTRACT
Oxidative stress, which is an early determinant of Alzheimer’s disease (AD), is involved in mediating neuronal apoptosis in Aβ-induced cell death. C60 fullerenes are known to behave like a “radical sponge” as they can sponge up free radicals and act more effectively than other antioxidants. PEG-C60-3, a C60 fullerene derivative, was investigated against β-amyloid (Aβ)25-35-induced toxicity toward Neuro-2A cells in this study. PEG-C60-3 reduced Aβ25-35-induced cytotoxicity, which showed an increasing cell viability with C60 and Aβ25-35 co-treated cells. Moreover, the intracellular reactive oxygen species (ROS) accumulation caused by Aβ-treated Neuro-2A cells was reduced by PEG-C60-3 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 C60 protective mechanism against Aβ25-35 treatment. The results offered new comprehension into the possible pathway of Aβ25-35 gene expression and C60 protective mechanism. With the understanding of the roles of Aβ and C60 in cells, we can hopefully provide insight on therapeutic design using C60 fullerene nanoparticles against Aβ-associated diseases.
Key words: apoptosis, amyloid, fullerene, reactive oxygen species (ROS)