Yaqin Zhao, Qiming Xu, Wei Xu, Dandan Wang, Jason Tan, Cuiqing Zhu and Xiangshi Tan
Metallomics, 2016,8, 644-647
DOI:
10.1039/C5MT00242G,
Communication
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 Aβ1–42 aggregation, protected from neurotoxicity of ROS induced by Cu2+ + Aβ1–42via 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.