PDF(Pubmed)
Abstract：
The extensive utilization of iron oxide nanoparticles in medical and life science domains has led to a substantial rise in both occupational and public exposure to these particles. The potential toxicity of nanoparticles to living organisms, their impact on the environment, and the associated risks to human health have garnered significant attention and come to be a prominent area in contemporary research. The comprehension of the potential toxicity of nanoparticles has emerged as a crucial concern to safeguard human health and facilitate the secure advancement of nanotechnology. As nanocarriers and targeting agents, the biocompatibility of them determines the use scope and application prospects, meanwhile surface modification becomes an important measure to improve the biocompatibility. Three different types of iron oxide nanoparticles (Fe3O4, Fe3O4@PDA and MSCM-Fe3O4@PDA) were injected into mice through the tail veins. The acute neurotoxicity of them in mice was evaluated by measuring the levels of autophagy and apoptosis in the brain tissues. Our data revealed that iron oxide nanoparticles could cause nervous system damage by regulating the ASK1/JNK signaling pathway. Apoptosis and autophagy may play potential roles in this process. Exposure to combined surface functionalization of mesenchymal stem cell membrane and polydopamine showed the neuroprotective effect and may alleviate brain nervous system disorders.
摘要：
氧化铁纳米颗粒在医学和生命科学领域的广泛利用导致职业和公众对这些颗粒的接触大幅增加。纳米粒子对生物体的潜在毒性，它们对环境的影响，与人类健康相关的风险已经引起了极大的关注，并成为当代研究的突出领域。对纳米颗粒潜在毒性的理解已成为保护人类健康和促进纳米技术安全发展的关键问题。作为纳米载体和靶向剂，生物相容性决定了其使用范围和应用前景,同时表面改性也成为提高生物相容性的重要措施。通过尾静脉将三种不同类型的氧化铁纳米颗粒（Fe3O4，Fe3O4@PDA和MSCM-Fe3O4@PDA）注射到小鼠体内。通过测定脑组织中自噬和细胞凋亡水平评价其对小鼠的急性神经毒性。我们的数据表明，氧化铁纳米颗粒可以通过调节ASK1/JNK信号通路引起神经系统损伤。细胞凋亡和自噬可能在这一过程中起着潜在的作用。暴露于间充质干细胞膜和聚多巴胺的联合表面功能化显示了神经保护作用，并可能减轻脑神经系统疾病。
