期刊
ACS APPLIED NANO MATERIALS
卷 5, 期 12, 页码 19025-19034出版社
AMER CHEMICAL SOC
DOI: 10.1021/acsanm.2c04938
关键词
brain-derived neurotrophic factor; mitochondria; nanoparticle; neuronal differentiation; oxidative stress
资金
- Japan Society for the Promotion of Science [21KD1002]
- Japan Ministry of Health, Labour and Welfare
- [19K19409]
Research has found that silver nanoparticles with a diameter of 10 nm can inhibit retinoic acid-induced neuronal differentiation. This inhibitory effect may be achieved through the oxidative stress pathway, induction of mitochondrial ROS production, and decreased expression of mitochondrial fusion-related genes.
Nanoparticles are being used in an increasing number of applications in a wide range of fields; however, these particles can migrate to the brain, raising concerns over their potential as risk factors of neurodevelopment disorders. Here, we examined the effects of silver nanoparticles with a diameter of 10 nm (nAg10) on neural differentiation in human-derived neuro-blastoma SH-SY5Y cells. SH-SY5Y cells treated with retinoic acid undergo neuronal differentiation characterized by increased expression of brain-derived neurotrophic factor (BDNF); however, co-treatment of these cells with retinoic acid (RA) and nAg10 significantly mitigated this RA-induced BDNF expression. RA-induced neurite outgrowth and extracellular secretion of dopamine were significantly suppressed by nAg10 in a concentration-dependent manner. Reactive oxygen species (ROS) production was enhanced in cells co-treated with RA and nAg10, and the expression level of BDNF was restored by co-treatment with nAg10 and an ROS inhibitor (N-acetylcysteine). nAg10-induced mitochondrial ROS production and decreased mitochondrial fusion-related gene expression. In summary, nAg10 suppressed retinoic acid-induced neuronal differentiation in SH-SY5Y cells via the oxidative stress pathway, induced mitochondrial ROS production, and decreased mitochondrial fusion-related gene expression.
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