探究氧化铈纳米颗粒抵御铜离子诱导的Aβ1-42神经细胞毒性的分子机制。
Probing the molecular mechanism of cerium oxide nanoparticles in protecting against the neuronal cytotoxicity of Aβ1-42 with copper ions.
作者信息
Zhao Yaqin, Xu Qiming, Xu Wei, Wang Dandan, Tan Jason, Zhu Cuiqing, Tan Xiangshi
机构信息
Department of Chemistry & Institutes of Biomedical Sciences, Fudan University, Shanghai 200433, China.
State Key Laboratory of Medical Neurobiology, Shanghai Medical College of Fudan University, Shanghai, China.
出版信息
Metallomics. 2016 Jul 13;8(7):644-7. doi: 10.1039/c5mt00242g.
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, 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 Cu(2+) + Aβ1-42via blocking the production of free radicals and scavenging the radicals with Ce(3+)/Ce(4+) catalytic cycles, which provides a valuable insight into CeONPs as a therapeutic intervention in oxidative damage in Alzheimer's disease.
通过Ru(phen)2dppz的光致发光、透射电子显微镜形态学、质谱分析、细胞活力测定、活性氧荧光测定和电子顺磁共振，系统研究了氧化铈纳米颗粒（CeONP）在保护神经元免受淀粉样肽和铜离子细胞毒性方面的分子机制。结果表明，CeONPs减少了Aβ1-42的聚集，通过阻断自由基的产生并利用Ce(3+)/Ce(4+)催化循环清除自由基，保护神经元免受Cu(2+) + Aβ1-42诱导的活性氧神经毒性，这为CeONPs作为阿尔茨海默病氧化损伤治疗干预提供了有价值的见解。
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