Extensive applications of ZnO NPs (zinc oxide nanoparticles) in daily life have created concern about their biotoxicity. Zinc oxide nanoparticles induce oxidative stress, inflammation, and apoptosis in neurons. Edaravone applies antioxidant agent and anti-inflammatory impacts in the different cells, as evaluated in both in vitro and in vivo experimental models. This study is designed to explore, how edaravone would avert mitochondrial impairment in human neuronal cells against ZnO NPs-induced toxicity. Accordingly, we analyzed here whether a pretreatment (for 24 h) with edaravone (10–100 μM) would enhance mitochondrial protection in the human neuroblastoma cells SH-SY5Y against ZnO NPs-induced toxicity. We found that edaravone at 25 μM averted the ZnO NPs-induced decrease in the amounts of adenosine triphosphate (ATP), just as on the activity of the complexes I and V. Also, edaravone induced an antioxidant activity by diminishing the levels of lipid peroxidation, protein carbonylation, and protein nitration in the mitochondrial membranes. Edaravone blocked the ZnO NPs-induced transcription factor nuclear factor-κB (NF-κB) upregulation. The inhibition of the heme oxygenase-1 (HO−1) enzyme by zinc protoporphyrin IX (ZnPP IX, 10 μM) smothered the preventive impacts brought about by edaravone with respect to mitochondrial function and inflammation. After this examination, it can be concluded that edaravone caused cytoprotective impacts in an HO−1-dependent manner in SH-SY5Y cells against ZnO NPs-induced toxicity.

ZnO NPs（氧化锌纳米颗粒）在日常生活中的广泛应用引起了人们对其生物毒性的担忧。氧化锌纳米颗粒在神经元中诱导氧化应激、炎症和细胞凋亡。如在体外和体内实验模型中评估的那样，依达拉奉在不同细胞中应用抗氧化剂和抗炎作用。本研究旨在探索依达拉奉如何避免人类神经元细胞中的线粒体损伤，从而对抗 ZnO NPs 诱导的毒性。因此，我们在此分析了用依达拉奉（10-100μM）预处理（24小时）是否会增强人神经母细胞瘤细胞SH-SY5Y中线粒体对ZnO NPs诱导的毒性的保护作用。我们发现 25 μM 的依达拉奉避免了 ZnO NPs 诱导的三磷酸腺苷 (ATP) 量的减少，就像复合物 I 和 V 的活性一样。此外，依达拉奉通过降低线粒体膜中脂质过氧化、蛋白质羰基化和蛋白质硝化的水平来诱导抗氧化活性。依达拉奉阻断了 ZnO NPs 诱导的转录因子核因子-κB (NF-κB) 上调。锌原卟啉 IX (ZnPP IX, 10 μM) 抑制血红素加氧酶-1 (HO-1) 抑制了依达拉奉对线粒体功能和炎症的预防作用。经过这次检查，可以得出结论，依达拉奉在 SH-SY5Y 细胞中以 HO-1 依赖性方式对 ZnO NPs 诱导的毒性产生细胞保护作用。和线粒体膜中的蛋白质硝化。依达拉奉阻断了 ZnO NPs 诱导的转录因子核因子-κB (NF-κB) 上调。锌原卟啉 IX (ZnPP IX, 10 μM) 对血红素加氧酶-1 (HO-1) 酶的抑制抑制了依达拉奉对线粒体功能和炎症的预防作用。经过这次检查，可以得出结论，依达拉奉在 SH-SY5Y 细胞中以 HO-1 依赖性方式对 ZnO NPs 诱导的毒性产生细胞保护作用。和线粒体膜中的蛋白质硝化。依达拉奉阻断了 ZnO NPs 诱导的转录因子核因子-κB (NF-κB) 上调。锌原卟啉 IX (ZnPP IX, 10 μM) 对血红素加氧酶-1 (HO-1) 酶的抑制抑制了依达拉奉对线粒体功能和炎症的预防作用。经过这次检查，可以得出结论，依达拉奉在 SH-SY5Y 细胞中以 HO-1 依赖性方式对 ZnO NPs 诱导的毒性产生细胞保护作用。10 μM) 抑制了依达拉奉对线粒体功能和炎症的预防作用。经过这次检查，可以得出结论，依达拉奉在 SH-SY5Y 细胞中以 HO-1 依赖性方式对 ZnO NPs 诱导的毒性产生细胞保护作用。10 μM) 抑制了依达拉奉对线粒体功能和炎症的预防作用。经过这次检查，可以得出结论，依达拉奉在 SH-SY5Y 细胞中以 HO-1 依赖性方式对 ZnO NPs 诱导的毒性产生细胞保护作用。