本研究探讨了氧化锌纳米颗粒 (ZnONP) 对氯化铝 (AlCl3) 介导的阿尔茨海默病 (AD) 样症状的潜在神经保护作用。将大鼠平均分为四个治疗组：对照组、ZnONPs（4 mg/kg b.wt.）、AlCl3（100 mg/kg b.wt.）和 ZnONPs  AlCl3 组。对大鼠进行连续 42 天的治疗。将 ZnONP 注射到 AlCl3 处理的大鼠体内，可以抑制皮质和海马组织中氧化应激的发展，神经元促氧化剂（丙二醛和一氧化氮）减少以及谷胱甘肽和过氧化氢酶水平增加就证明了这一点。此外，ZnONPs 注射液通过降低肿瘤坏死因子-α 和白细胞介素-1β 的水平，显示出对 AlCl3 的抗炎功效。此外，ZnONPs 预处理可通过降低促凋亡 caspase-3 的水平并增强抗凋亡 B 细胞淋巴瘤 2 的水平来防止神经元细胞损失。此外，ZnONPs 还可改善受干扰的乙酰胆碱酯酶活性、单胺（去甲肾上腺素、多巴胺和血清素）、 AlCl3 暴露后产生兴奋性氨基酸（谷氨酸和天冬氨酸）和抑制性氨基酸（GABA 和甘氨酸）。这些发现表明，ZnONPs 可能具有作为替代疗法的潜力，通过表现出抗氧化、抗炎、抗凋亡和神经调节作用，最大限度地减少或预防 AD 模型中的神经缺陷。© 2024。作者，独家授予 Springer Science Business Media, LLC（Springer Nature 的一部分）的许可。

The present investigation explored the potential neuroprotective role of zinc oxide nanoparticles (ZnONPs) on aluminum chloride (AlCl3)-mediated Alzheimer's disease (AD)-like symptoms. Rats were distributed into four treatment groups equally: control, ZnONPs (4 mg/kg b.wt.), AlCl3 (100 mg/kg b.wt.), and ZnONPs + AlCl3 groups. Rats were treated for 42 consecutive days. ZnONPs injection into AlCl3-treated rats suppressed the development of oxidative challenge in the cortical and hippocampal tissues, as demonstrated by the decreased neuronal pro-oxidants (malondialdehyde and nitric oxide), and the increased glutathione and catalase levels. Additionally, ZnONPs injection showed anti-inflammatory potency in response to AlCl3 by decreasing levels of tumor necrosis factor-α and interleukin-1β. Moreover, pretreatment with ZnONPs prevented neuronal cell loss by decreasing the level of pro-apoptotic caspase-3 and enhancing the anti-apoptotic B cell lymphoma 2. Furthermore, ZnONPs ameliorated the disturbed acetylcholinesterase activity, monoamines (norepinephrine, dopamine, and serotonin), excitatory (glutamic and aspartic acids), and inhibitory amino acids (GABA and glycine) in response to AlCl3 exposure. These findings indicate that ZnONPs may have the potential as an alternative therapy to minimize or prevent the neurological deficits in AD model by exhibiting antioxidative, anti-inflammation, anti-apoptosis, and neuromodulatory effects.© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.