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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Effects of silica nanoparticles on endolysosome function in primary cultured neurons
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Effects of silica nanoparticles on endolysosome function in primary cultured neurons

机译：二氧化硅纳米粒子对原发性培养神经元底糖体功能的影响

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Silica nanoparticles (SiNPs) have been used as vehicles for drug delivery, molecular detection, and cellular manipulations in nanoneuromedicine. SiNPs may cause adverse effects in the brain including neurotoxicity, neuroinflammation, neurodegeneration, and enhancing levels of amyloid beta (A beta) protein-all pathological hallmarks of Alzheimer's disease. Therefore, the extent to which SiNPs influence A beta generation and the underlying mechanisms by which this occurs deserve investigation. Our studies were focused on the effects of SiNPs on endolysosomes which uptake, traffic, and mediate the actions of SiNPs. These organelles are also where amyloidogenesis largely originates. We found that SiNPs, in primary cultured hippocampal neurons, accumulated in endolysosomes and caused a rapid and persistent deacidification of endolysosomes. SiNPs significantly reduced endolysosome calcium stores as indicated by a significant reduction in the ability of the lysosomotropic agent glycyl-L-phenylalanine 2-naphthylamide (GPN) to release calcium from endolysosomes. SiNPs increased A beta(1-40) secretion, whereas 2 agents that acidified endolysosomes, ML-SA1 and CGS21680, blocked SiNP-induced deacidification and increased generation of A beta(1-40). Our findings suggest that SiNP-induced deacidification of and calcium release from endolysosomes might be mechanistically linked to increased amyloidogenesis. The use of SiNPs might not be the best nanomaterial for therapeutic strategies against Alzheimer's disease and other neurological disorders linked to endolysosome dysfunction.
机译：二氧化硅纳米颗粒（SINPS）已被用作用于药物递送，分子检测和纳米核细胞的细胞操纵的车辆。 Sinps可能导致大脑中的不良反应，包括神经毒性，神经炎症，神经变性，增强淀粉样蛋白β（Aβ）蛋白的水平 - 阿尔茨海默病的所有病理标志。因此，SINPS影响β生成的程度和这种情况发生的潜在机制值得调查。我们的研究侧重于SINPS对鼻内肌肉的影响，其吸收，交通和调节SINPS的行为。这些细胞器也在其中淀粉样品发生在很大源自源极。我们发现SINPS，在初级培养的海马神经元中，积累在底糖体中，并引起了底糖苷的快速和持续的脱髓。 SINPS显着降低了内溶血体钙储存，如溶酶体脱脂剂甘氨酸甘氨酸甘氨酸甘氨酸（GPN）释放出从底糖苷释放钙的能力的显着降低。 SINPS增加了β（1-40）分泌，而2个试剂酸化底糖瘤，ML-SA1和CGS21680，阻断SINP诱导的脱酸和β（1-40）的产生增加。我们的研究结果表明，SINP诱导的底糖瘤的钙释放和钙释放可能与增加的淀粉样蛋白生成增加。 SINPS的使用可能不是针对阿尔茨海默病的治疗策略的最佳纳米材料，以及与内炎功能障碍相关的其他神经系统疾病。

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