Probing the molecular mechanism of cerium oxide nanoparticles in protecting against the neuronal cytotoxicity of Aβ1–42 with copper ions

Abstract

The molecular mechanism of CeONP in protecting against neuronal cytotoxicity from amyloid peptides and copper ions was investigated systematically by photoluminescence of [Ru(phen)₂dppz]²⁺, morphology of TEM, mass spectroscopy, cell viability assay, ROS fluorescence assay, and EPR. The results revealed that CeONPs reduced Aβ_1–42 aggregation, protected from neurotoxicity of ROS induced by Cu²⁺ + Aβ_1–42via blocking the production of free radicals and scavenging the radicals with Ce³⁺/Ce⁴⁺ catalytic cycles, which provides a valuable insight into CeONPs as a therapeutic intervention in oxidative damage in Alzheimer's disease.