Hanzha Vita V, Rozumna Nataliia M, Kravenska Yevheniia V, Spivak Mykola Ya, Lukyanetz Elena A
Department of Biophysics of Ion Channels, Bogomoletz Institute of Physiology, The National Academy of Sciences of Ukraine (NASU), Kyiv, Ukraine.
Danylo Zabolotny Institute of Microbiology and Virology, The National Academy of Sciences of Ukraine (NASU), Kyiv, Ukraine.
Front Cell Neurosci. 2023 Mar 16;17:1131168. doi: 10.3389/fncel.2023.1131168. eCollection 2023.
The possibilities of using nanoparticle materials based on cerium dioxide (CNPs) are exciting since they are low toxic and have specific redox, antiradical properties. It can be supposed that CNPs' biomedical use is also relevant in neurodegenerative diseases, especially Alzheimer's disease (AD). AD is known as the pathologies leading to progressive dementia in the elderly. The factor that provokes nerve cell death and cognitive impairment in AD is the pathological accumulation of beta-amyloid peptide (Aβ) in the brain tissue. In our studies, we examined the impact of Aβ 1-42 on neuronal death and evaluated the potential neuroprotective properties of CNPs during AD modeling in cell culture. Our findings show that, under AD modeling conditions, the number of necrotic neurons increased from 9.4% in the control to 42.7% when Aβ 1-42 was used. In contrast, CNPs alone showed low toxicity, with no significant increase in the number of necrotic cells compared to control conditions. We further explored the potential of CNPs as a neuroprotective agent against Aβ-induced neuronal death. We found that introducing CNPs 24 h after Aβ 1-42 incubation or prophylactically incubating hippocampal cells with CNPs 24 h before amyloid administration significantly reduced the percentage of necrotic cells to 17.8 and 13.3%, respectively. Our results suggest that CNPs in the cultural media can significantly reduce the number of dead hippocampal neurons in the presence of Aβ, highlighting their neuroprotective properties. These findings suggest that CNPs may hold promise for developing new treatments for AD based on their neuroprotective properties.
基于二氧化铈的纳米颗粒材料(CNPs)具有令人兴奋的应用潜力,因为它们毒性低且具有特定的氧化还原、抗自由基特性。可以推测,CNPs在生物医学领域的应用对于神经退行性疾病,尤其是阿尔茨海默病(AD)也具有重要意义。AD是导致老年人进行性痴呆的病理状态。在AD中引发神经细胞死亡和认知障碍的因素是脑组织中β-淀粉样肽(Aβ)的病理性积累。在我们的研究中,我们研究了Aβ 1-42对神经元死亡的影响,并评估了在细胞培养中进行AD建模时CNPs的潜在神经保护特性。我们的研究结果表明,在AD建模条件下,使用Aβ 1-42时,坏死神经元的数量从对照组的9.4%增加到了42.7%。相比之下,单独的CNPs显示出低毒性,与对照条件相比,坏死细胞数量没有显著增加。我们进一步探索了CNPs作为抗Aβ诱导的神经元死亡的神经保护剂的潜力。我们发现,在Aβ 1-42孵育24小时后引入CNPs,或者在给予淀粉样蛋白前24小时用CNPs预防性孵育海马细胞,可将坏死细胞的百分比分别显著降低至17.8%和13.3%。我们的结果表明,在存在Aβ的情况下,培养基中的CNPs可以显著减少死亡的海马神经元数量,突出了它们的神经保护特性。这些发现表明,基于其神经保护特性,CNPs可能为开发AD的新治疗方法带来希望。