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Synthesis of Cerium Oxide Nanoparticles and the Regulatory Effects on RGC-5Cell Apoptosis

Author: WangXingHua
Tutor: JiangFaGang
School: Huazhong University of Science and Technology
Course: Ophthalmology
Keywords: Cerium oxide nanoparticles Retinal ganglion cells Oxidative stress Apoptosis Neuroprotection
CLC: R943
Type: PhD thesis
Year: 2013
Downloads: 1
Quote: 0
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Abstract


Purpose:Oxidative stress participates in the pathogenesis of retinal ganglion (RGCs) death in various ocular diseases. Cerium oxide nanoparticles (CNPs) showed excellent antioxidative capacity and exerted significant neuroprotection in several models of neuronal injury. The present study aimed to confirm the neuroprotective effects of CNPs against the oxidative injuries to RGCs, and further elucidate the potential mechanisms.Methods:CNPs were synthesized by using a chemical precipitation method, and characterized for the particle diameter, mixed valence state and crystal lattice by using high resolution transmission electronmicroscopy (HRTEM) and other assays. Oxidative injury to RGC-5(a RGCs cell line) induced by hydrogen peroxide was chosen as the neuronal injury model in vitro. The viability of RGC-5, apoptotic morphology and quantification analysis were perfrmed in different groups. Furthermore, the intracellular oxygen radicals, defensive anti-oxidative enzymes, mitochondrial membrane potential, and the expression of cytochrome c, Bax, Bcl-2and caspase-3were dected to certify the mechanisms.Results:The particle diameter of CNPs obtained was5-10nm. CNPs dispersed well in normal saline and showed the mixed valence state of+3and+4. CNPs promoted RGC-5viability after H2O2stimulation, inhibited the morphology alternation of cellular apoptosis, and decreased the apoptotic rate of RGC-5significantly. Furthermore, CNPs decreased the intracellular oxygen radical after H2O2challenge, and increased the concentrations of SOD, GPx and catalase. CNPs also maintained the mitochondrial membrane potential, and reversed the tendency of cytochrome c release from mitochondria to cytoplasm. The ratio of Bax/Bcl-2decreased due to CNPs intervention, and caspase-3expression were inhibited by CNPs significantly.Conclusions:CNPs exerted significant neuroprotection against RGCs apoptosis induced by oxidative injury, which might related to the antioxidative activity of CNPs. The results pointed to a novel therapeutic path for RGCs neuroprotection.

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