Zinc Oxide Nanoparticles Attenuated Neurochemical and Histopathological Alterations Associated with Aluminium Chloride Intoxication in Rats

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.

Keywords: Alzheimer’s disease; Apoptosis; Neuroinflammation; Neurotransmission; Oxidative challenge; Zinc oxide nanoparticles.