Zhang Lan, Zhao Jinjin, Guo Xinyue, Ge Cuicui, Chang Lijun, Gao Xiaocheng, Huang Tao, Wang Yanhong, Shang Nan, Niu Qiao, Zhang Qinli
Department of Occupational Health, School of Public Health, Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Department of Pharmacy, First Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China.
Neurotox Res. 2022 Oct;40(5):1191-1207. doi: 10.1007/s12640-022-00549-9. Epub 2022 Aug 9.
The aim of this study was to explore the influence of the neurotoxicity of nanoalumina on primarily cultured neurons. Normal control, particle size control, aluminum, micron-alumina, and nanoalumina at 50-nm and 13-nm particle sizes were included as subjects to evaluate the level of apoptosis, necrosis, and autophagy in primarily cultured neurons and further explore the mitophagy induced by nanoalumina. The results demonstrated that nanoalumina could induce neuronal cell apoptosis, necrosis, and autophagy, among which autophagy was the most notable. When the autophagy inhibitor was added to the nanoalumina-treated group, it significantly downregulated the protein expression levels of Beclin-1 and LC3II/LC3. Observation under a transmission electron microscope and a fluorescence microscope revealed mitophagy characteristics induced by nanoalumina. Additionally, the neurotoxicological effects induced by nanoalumina were more significant than those induced by aluminum and in a particle size-dependent manner.
本研究的目的是探讨纳米氧化铝的神经毒性对原代培养神经元的影响。将正常对照组、粒径对照组、铝、微米级氧化铝以及粒径为50纳米和13纳米的纳米氧化铝作为研究对象，以评估原代培养神经元中细胞凋亡、坏死和自噬的水平，并进一步探究纳米氧化铝诱导的线粒体自噬。结果表明，纳米氧化铝可诱导神经元细胞凋亡、坏死和自噬，其中自噬最为显著。当向纳米氧化铝处理组添加自噬抑制剂时，Beclin-1和LC3II/LC3的蛋白表达水平显著下调。透射电子显微镜和荧光显微镜观察显示纳米氧化铝诱导了线粒体自噬特征。此外，纳米氧化铝诱导的神经毒理学效应比铝诱导的效应更显著，且呈粒径依赖性。
