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

• Published in: Neurochemical research Vol. 44; no. 7; pp. 1549 - 1566
• Main Authors: Zheng, Yafei, Wu, Yuyun, Liu, Ying, Guo, Zhirui, Bai, Tingting, Zhou, Ping, Wu, Jin, Yang, Qin, Liu, Zhengxia, Lu, Xiang
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.07.2019; Springer Nature B.V
• Subjects: AKT protein; Animals; Antioxidants - adverse effects; Antioxidants - chemistry; Antioxidants - therapeutic use; Apoptosis; Apoptosis - drug effects; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell Survival - drug effects; Cell viability; Cells, Cultured; Cerebral Cortex - drug effects; Chemical compounds; Deprivation; Electron transport; Glucose; Glucose - metabolism; Glycogen Synthase Kinase 3 beta - metabolism; Gold; Gold - adverse effects; Gold - chemistry; Gold - therapeutic use; Inflammation - drug therapy; Injuries; Ischemia; Membrane Potential, Mitochondrial - drug effects; Metal Nanoparticles - adverse effects; Metal Nanoparticles - chemistry; Metal Nanoparticles - therapeutic use; Mitochondria; Mitochondria - drug effects; Nanoparticles; Neurochemistry; Neurology; Neurons; Neurons - cytology; Neurons - drug effects; Neuroprotective Agents - adverse effects; Neuroprotective Agents - chemistry; Neuroprotective Agents - therapeutic use; Neurosciences; Original Paper; Oxidative stress; Oxidative Stress - drug effects; Oxygen; Oxygen - metabolism; Particle Size; Pharmacology; Proto-Oncogene Proteins c-akt - metabolism; Rats, Sprague-Dawley; Reperfusion; Reperfusion Injury - drug therapy; Respiration; Signal Transduction - drug effects; Signaling; Oxidative stress; Neuronal apoptosis; Mitochondria; Ischemic stroke; Primary rat cortical neurons; Gold nanoparticles
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-019-02776-7

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.