ZOMEC via the p-Akt/Nrf2 Pathway Restored PTZ-Induced Oxidative Stress-Mediated Memory Dysfunction in Mouse Model

Abstract

A new mechanistic approach to overcome the neurodegenerative disorders caused by oxidative stress in Alzheimer's disease (AD) is highly stressed in this article. Thus, a newly formulated drug (zinc ortho-methyl carbonodithioate (ZOMEC)) was investigated for five weeks on seven-week-old BALB/c male mice. ZOMEC 30 mg/kg was postadministered intraperitoneally during the third week of pentylenetetrazole (PTZ) injection. The brain homogenates of the mice were evaluated for their antioxidant potential for ZOMEC. The results including catalase (CAT), glutathione S transferase (GST), and lipid peroxidation (LPO) demonstrated that ZOMEC significantly reverted the oxidative stress stimulated by PTZ in the mouse brain. ZOMEC upregulated p-Akt/Nrf-2 pathways (also supported by molecular docking methods) to revoke PTZ-induced apoptotic protein markers. ZOMEC reversed PTZ-induced neuronal synapse deficits, improved oxidative stress-aided memory impairment, and inhibited the amyloidogenic pathway in mouse brains. The results suggested the potential of ZOMEC as a new, safe, and neurotherapeutic agent to cure neurodegenerative disorders by decreasing AD-like neuropathology in the animal PTZ model.