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金纳米粒子对大鼠皮质神经元氧葡萄糖剥夺/再灌注损伤的内在作用。

Intrinsic Effects of Gold Nanoparticles on Oxygen-Glucose Deprivation/Reperfusion Injury in Rat Cortical Neurons.

机构信息

Department of Geriatrics, The Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210003, Jiangsu, People's Republic of China.

Key Laboratory for Aging & Disease, Nanjing Medical University, Nanjing, 210003, Jiangsu, People's Republic of China.

出版信息

Neurochem Res. 2019 Jul;44(7):1549-1566. doi: 10.1007/s11064-019-02776-7. Epub 2019 May 15.

Abstract

This study aimed to investigate the potential effects of gold nanoparticles (Au-NPs) on rat cortical neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R) and to elucidate the corresponding mechanisms. Primary rat cortical neurons were exposed to OGD/R, which is commonly used in vitro to mimic ischemic injury, and then treated with 5- or 20-nm Au-NPs. We then evaluated cell viability, apoptosis, oxidative stress, and mitochondrial respiration in these neurons. We found that 20-nm Au-NPs increased cell viability, alleviated neuronal apoptosis and oxidative stress, and improved mitochondrial respiration after OGD/R injury, while opposite effects were observed for 5-nm Au-NPs. In terms of the underlying mechanisms, we found that Au-NPs could regulate Akt signaling. Taken together, these results show that 20-nm Au-NPs can protect primary cortical neurons against OGD/R injury, possibly by decreasing apoptosis and oxidative stress, while activating Akt signaling and mitochondrial pathways. Our results suggest that Au-NPs may be potential therapeutic agents for ischemic stroke.

摘要

本研究旨在探讨金纳米粒子(Au-NPs)对氧葡萄糖剥夺/再灌注(OGD/R)暴露的大鼠皮质神经元的潜在影响,并阐明相应的机制。原代大鼠皮质神经元暴露于 OGD/R,这是体外模拟缺血损伤的常用方法,然后用 5nm 或 20nm Au-NPs 处理。然后,我们评估了这些神经元中的细胞活力、细胞凋亡、氧化应激和线粒体呼吸。我们发现 20nm Au-NPs 增加了细胞活力,减轻了神经元凋亡和氧化应激,并改善了 OGD/R 损伤后的线粒体呼吸,而 5nm Au-NPs 则产生了相反的效果。就潜在机制而言,我们发现 Au-NPs 可以调节 Akt 信号。总之,这些结果表明 20nm Au-NPs 可以保护原代皮质神经元免受 OGD/R 损伤,可能通过减少细胞凋亡和氧化应激,同时激活 Akt 信号和线粒体途径。我们的研究结果表明,Au-NPs 可能是治疗缺血性中风的潜在治疗剂。

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