Zinc Ortho Methyl Carbonodithioate Improved Pre and Post-Synapse Memory Impairment via SIRT1/p-JNK Pathway against Scopolamine in Adult Mice

Alzheimer’s disease (AD) is globally recognized as a prominent cause of dementia for which efficient treatment is still lacking. New candidate compounds that are biologically potent are regularly tested. We, therefore, hypothesized to study the neuroprotective potential of Zinc Ortho Methyl Carbonodithioate (thereafter called ZOMEC) against Scopolamine (SCOP) induced Alzheimer’s disease (AD) model using adult albino mice. We post-administered ZOMEC (30 mg/Kg) into two group of mice for three weeks on daily basis that received either 0.9% saline or SCOP (1 mg/Kg) for initial two weeks. The other two groups of mice received 0.9% saline and SCOP (1 mg/Kg) respectively. After memory related behavioral analysis the brain homogenates were evaluated for the antioxidant potential of ZOMEC and multiple protein markers were examined through western blotting. Our results provide enough evidences that ZOMEC decrease oxidative stress by increasing catalase (CAT) and glutathione S transferase (GST) and decreasing the lipid peroxidation (LPO). The SIRT1 and pre and post synaptic marker proteins, synaptophysin (SYP) as well as post synaptic density protein (PSD-95) expression were also enhanced upon ZOMEC treatment. Furthermore, memory impairment was rescued and ZOMEC appreciably abrogated the Aβ accumulation, BACE1 expression C and the p-JNK pathway. The inflammatory protein markers, NF-kβ and IL-1β in ZOMEC treated mice were also comparable with control group. The predicted interaction of ZOMEC with SIRT1 was further confirmed by molecular docking. These findings thus provide initial reports on efficacy of ZOMEC in SCOP induced AD model. Graphical Abstract.

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:18

Enthalten in:

Journal of neuroImmune pharmacology - 18(2023), 1-2 vom: 01. Juni, Seite 183-194

Sprache:

Englisch

Beteiligte Personen:

Jahan, Rifat [VerfasserIn]
Yousaf, Mohammad [VerfasserIn]
Khan, Hamayun [VerfasserIn]
Shah, Shahid Ali [VerfasserIn]
Khan, Abdul Aziz [VerfasserIn]
Bibi, Nousheen [VerfasserIn]
Javed, Fatima [VerfasserIn]
Ijaz, Musarrat [VerfasserIn]
Ali, Arif [VerfasserIn]
Wei, Dong-Qing [VerfasserIn]

Links:

Volltext [lizenzpflichtig]

Themen:

Alzheimer's disease
P-JNK
PSD95
SIRT1
SYP

Anmerkungen:

© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

doi:

10.1007/s11481-023-10067-w

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

OLC2145447695

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