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Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction
Alzheimer’s disease (AD) is one of the primary health problems linked to the decrease of acetylcholine in cholinergic neurons and elevation in oxidative stress. Myco-fabrication of ZnO-NPs revealed excellent biological activities, including anti-inflammatory and acetylcholinesterase inhibitory poten...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Netherlands
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10684416/ https://www.ncbi.nlm.nih.gov/pubmed/37556014 http://dx.doi.org/10.1007/s10534-023-00525-6 |
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author | Abd Elmonem, Hanan A. Morsi, Reham M. Mansour, Doaa S. El-Sayed, El-Sayed R. |
author_facet | Abd Elmonem, Hanan A. Morsi, Reham M. Mansour, Doaa S. El-Sayed, El-Sayed R. |
author_sort | Abd Elmonem, Hanan A. |
collection | PubMed |
description | Alzheimer’s disease (AD) is one of the primary health problems linked to the decrease of acetylcholine in cholinergic neurons and elevation in oxidative stress. Myco-fabrication of ZnO-NPs revealed excellent biological activities, including anti-inflammatory and acetylcholinesterase inhibitory potentials. This study aims to determine if two distinct doses of myco-fabricated ZnO-NPs have a positive impact on behavioral impairment and several biochemical markers associated with inflammation and oxidative stress in mice that have been treated by aluminum chloride (AlCl(3)) to induce AD. Sixty male mice were haphazardly separated into equally six groups. Group 1 was injected i.p. with 0.5 ml of deionized water daily during the experiment. Mice in group 2 received AlCl(3) (50 mg/kg/day i.p.). Groups 3 and 4 were treated i.p. with 5 and 10 mg/kg/day of ZnO-NPs only, respectively. Groups 5 and 6 were given i.p. 5 and 10 mg/kg/day ZnO-NPs, respectively, add to 50 mg/kg/day AlCl(3). Results showed that the AlCl(3) caused an increase in the escape latency time and a reduction in the time spent in the target quadrant, indicating a decreased improvement in learning and memory. Moreover, acetylcholinesterase enzyme (AChE) activity and malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin 1β (IL-1β) levels were significantly increased, and the content of glutathione (GSH), activities of superoxide dismutase (SOD), catalase (CAT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), as well as levels of serotonin and dopamine, were decreased in brain tissues only in AlCl(3) treated mice. However, treatment of mice with myco-fabrication of ZnO-NPs at doses of 5 or 10 mg/kg improves learning and memory function through ameliorate all the previous parameters in the AD mice group. The low dose of 5 mg/kg is more effective than a high dose of 10 mg/kg. In accordance with these findings, myco-fabricated ZnO-NPs could enhance memory and exhibit a protective influence against memory loss caused by AlCl(3). |
format | Online Article Text |
id | pubmed-10684416 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Springer Netherlands |
record_format | MEDLINE/PubMed |
spelling | pubmed-106844162023-11-30 Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction Abd Elmonem, Hanan A. Morsi, Reham M. Mansour, Doaa S. El-Sayed, El-Sayed R. Biometals Research Alzheimer’s disease (AD) is one of the primary health problems linked to the decrease of acetylcholine in cholinergic neurons and elevation in oxidative stress. Myco-fabrication of ZnO-NPs revealed excellent biological activities, including anti-inflammatory and acetylcholinesterase inhibitory potentials. This study aims to determine if two distinct doses of myco-fabricated ZnO-NPs have a positive impact on behavioral impairment and several biochemical markers associated with inflammation and oxidative stress in mice that have been treated by aluminum chloride (AlCl(3)) to induce AD. Sixty male mice were haphazardly separated into equally six groups. Group 1 was injected i.p. with 0.5 ml of deionized water daily during the experiment. Mice in group 2 received AlCl(3) (50 mg/kg/day i.p.). Groups 3 and 4 were treated i.p. with 5 and 10 mg/kg/day of ZnO-NPs only, respectively. Groups 5 and 6 were given i.p. 5 and 10 mg/kg/day ZnO-NPs, respectively, add to 50 mg/kg/day AlCl(3). Results showed that the AlCl(3) caused an increase in the escape latency time and a reduction in the time spent in the target quadrant, indicating a decreased improvement in learning and memory. Moreover, acetylcholinesterase enzyme (AChE) activity and malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin 1β (IL-1β) levels were significantly increased, and the content of glutathione (GSH), activities of superoxide dismutase (SOD), catalase (CAT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), as well as levels of serotonin and dopamine, were decreased in brain tissues only in AlCl(3) treated mice. However, treatment of mice with myco-fabrication of ZnO-NPs at doses of 5 or 10 mg/kg improves learning and memory function through ameliorate all the previous parameters in the AD mice group. The low dose of 5 mg/kg is more effective than a high dose of 10 mg/kg. In accordance with these findings, myco-fabricated ZnO-NPs could enhance memory and exhibit a protective influence against memory loss caused by AlCl(3). Springer Netherlands 2023-08-09 2023 /pmc/articles/PMC10684416/ /pubmed/37556014 http://dx.doi.org/10.1007/s10534-023-00525-6 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Abd Elmonem, Hanan A. Morsi, Reham M. Mansour, Doaa S. El-Sayed, El-Sayed R. Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction |
title | Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction |
title_full | Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction |
title_fullStr | Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction |
title_full_unstemmed | Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction |
title_short | Myco-fabricated ZnO nanoparticles ameliorate neurotoxicity in mice model of Alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction |
title_sort | myco-fabricated zno nanoparticles ameliorate neurotoxicity in mice model of alzheimer’s disease via acetylcholinesterase inhibition and oxidative stress reduction |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10684416/ https://www.ncbi.nlm.nih.gov/pubmed/37556014 http://dx.doi.org/10.1007/s10534-023-00525-6 |
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