Abstract：
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.
摘要：
本研究探讨了氧化锌纳米颗粒（ZnONPs）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（4mg/kgb.wt.),AlCl3(100mg/kgb.wt.),和ZnONPs+AlCl3基团。大鼠连续治疗42天。ZnONPs注射到AlCl3处理的大鼠中抑制了皮质和海马组织中氧化攻击的发展，正如神经元前氧化剂（丙二醛和一氧化氮）减少所证明的那样，谷胱甘肽和过氧化氢酶水平升高。此外,通过降低肿瘤坏死因子-α和白介素-1β的水平，ZnONPs注射显示出对AlCl3的抗炎效力。此外，用ZnONPs预处理通过降低促凋亡caspase-3的水平和增强抗凋亡B细胞淋巴瘤2来防止神经元细胞丢失。此外，ZnONPs改善了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)，兴奋性（谷氨酸和天冬氨酸），和抑制性氨基酸（GABA和甘氨酸）响应于AlCl3暴露。这些发现表明，ZnONPs可能具有作为替代疗法的潜力，通过表现出抗氧化作用来最小化或预防AD模型中的神经功能缺损。抗炎，抗凋亡，和神经调节效应。
