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Cerium oxide nanoparticles prevent apoptosis in primary cortical culture by stabilizing mitochondrial membrane potential

机译:氧化铈纳米粒子通过稳定线粒体膜电位来防止原代皮质培养物中的细胞凋亡

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Cerium oxide nanoparticles (CNPs) of spherical shape have unique antioxidant capacity primarily due to alternating + 3 and + 4 oxidation states and crystal defects. Several studies revealed the protective efficacies of CNPs in cells and tissues against the oxidative damage. However, its effect on mitochondrial functioning, downstream effectors of radical burst and apoptosis remains unknown. In this study, we investigated whether CNPs treatment could protect the primary cortical cells from loss of mitochondrial membrane potential (Delta psi(m)) and Delta psi(m)-dependent cell death. CNPs with spherical morphology and size range 7-10 nm were synthesized and utilized at a concentration of 25 nM on primary neuronal culture challenged with 50 mu M of hydrogen peroxide (H2O2). We showed that optimal dose of CNPs minimized ROS content of the cells and also curbed related surge in cellular calcium flux. Importantly, CNPs treatment prevented apoptotic loss of cell viability. Reduction in the apoptosis could be successfully attributed to the maintenance of Delta psi(m) and restoration of major redox equivalents NADH/NAD(+) ratio and cellular ATP. These findings, therefore, suggest possible route of CNPs protective efficacies in primary cortical culture.
机译:球形的氧化铈纳米颗粒(CNP)具有独特的抗氧化能力,这主要是由于交替的+ 3和+ 4氧化态和晶体缺陷。几项研究揭示了CNP在细胞和组织中对氧化损伤的保护作用。然而,其对线粒体功能,自由基爆发的下游效应子和细胞凋亡的作用仍然未知。在这项研究中,我们调查了CNPs处理是否可以保护原代皮质细胞免受线粒体膜电位(Delta psi(m))和Delta psi(m)依赖性细胞死亡的损害。合成具有球形形态和尺寸范围为7-10 nm的CNP,并以25 nM的浓度将其用于经50μM过氧化氢(H2O2)攻击的原代神经元培养物中。我们表明,最佳剂量的CNP可使细胞的ROS含量降至最低,并抑制细胞钙通量的相关激增。重要的是,CNPs处理可防止细胞凋亡的凋亡。凋亡的减少可以成功地归因于维持Delta psi(m)和恢复主要的氧化还原当量NADH / NAD(+)比率和细胞ATP。因此,这些发现表明在原代皮层培养中CNPs保护作用的可能途径。

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