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Published in: Journal of Nanoparticle Research 11/2014

01-11-2014 | Research Paper

Cerium oxide nanoparticles protect primary mouse bone marrow stromal cells from apoptosis induced by oxidative stress

Authors: Qun Zhang, Kun Ge, Jianlei Duan, Shizhu Chen, Ran Zhang, Cuimiao Zhang, Shuxiang Wang, Jinchao Zhang

Published in: Journal of Nanoparticle Research | Issue 11/2014

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Abstract

Cerium oxide nanoparticles (nanoceria) have been widely used in industries and biomedical fields due to its unique properties. Previous biodistribution studies of nanoceria in vivo have shown that they are accumulated in the bone of mice after intravenous administration, about 20 % of the total intake, however, the potential effect and the mechanism of nanoceria on bone metabolism are not well-understood. Our results showed that both 25 and 50 nm nanceria decreased the damage of cell viability induced by H2O2 in a dose-dependent manner. The apoptosis ratio of pre-incubated group with nanoceria was lower than the H2O2 group. The cellular uptake studies indicated that there was a dose-dependent accumulation of both two size nanoparticles in bone marrow stromal cells. Nanoceria could be uptaken by cells due to the synergistic effect of multiple endocytosis mechanisms, and then evenly distributed in the cytoplasm without entering the nucleus. Our results suggest that nanoceria could reduce intracellular ROS level induced by H2O2 in a dose-dependent manner, moreover, maintain the normal function of mitochondria, suggesting nanoceria may have potent applications for preventing or treating osteoporosis.

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Metadata
Title
Cerium oxide nanoparticles protect primary mouse bone marrow stromal cells from apoptosis induced by oxidative stress
Authors
Qun Zhang
Kun Ge
Jianlei Duan
Shizhu Chen
Ran Zhang
Cuimiao Zhang
Shuxiang Wang
Jinchao Zhang
Publication date
01-11-2014
Publisher
Springer Netherlands
Published in
Journal of Nanoparticle Research / Issue 11/2014
Print ISSN: 1388-0764
Electronic ISSN: 1572-896X
DOI
https://doi.org/10.1007/s11051-014-2697-3

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