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

Autor: Attia FM; Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo, Egypt., Kassab RB; Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo, Egypt. ramikassab@mail.muni.cz.; Biology Department, Faculty of Science and Arts, Almakhwah, Al Baha University, Al Baha, Saudi Arabia. ramikassab@mail.muni.cz., Ahmed-Farid OA; Physiology Department, Egyptian Drug Authority, Giza, Egypt., Abdel Moneim AE; Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo, Egypt., El-Yamany NA; Zoology and Entomology Department, Faculty of Science, Helwan University, Cairo, Egypt.
Jazyk: angličtina
Zdroj: Biological trace element research [Biol Trace Elem Res] 2024 Jul 04. Date of Electronic Publication: 2024 Jul 04.
DOI: 10.1007/s12011-024-04292-4
Abstrakt: The present investigation explored the potential neuroprotective role of zinc oxide nanoparticles (ZnONPs) on aluminum chloride (AlCl 3 )-mediated Alzheimer's disease (AD)-like symptoms. Rats were distributed into four treatment groups equally: control, ZnONPs (4 mg/kg b.wt.), AlCl 3 (100 mg/kg b.wt.), and ZnONPs + AlCl 3 groups. Rats were treated for 42 consecutive days. ZnONPs injection into AlCl 3 -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 AlCl 3 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 AlCl 3 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.)
Databáze: MEDLINE
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