Effect of Alcea Aucheri (Bioss.) Alef Extract Against Scopolamine-Induced Memory Impairment in Rats Publisher Pubmed



T Mombeini TAJMAH ; Hg Pourbadie Hamid GHOLAMI ; M Kamalinejad MOHAMMAD ; Ar Dehpour Ahmad REZA ; S Mazloumi SOROUSH ; R Hamidian REZA
Source: Behavioural Pharmacology Published:2025

Abstract

Memory impairment is a core feature of neurodegenerative diseases such as Alzheimer’s disease, often modeled using scopolamine-induced cognitive dysfunction in animals. While Alcea aucheri (Boiss.) Alef has demonstrated anxiolytic properties, but its potential impact on cognitive function, particularly memory, remains unexplored. This study investigates the effects of extract of flower of Alcea aucheri (EFA) on cognitive performance in scopolamine-free rats and in a scopolamine-induced memory impairment model. Male Wistar rats were administered EFA [17.5–700 mg/kg, intraperitoneally (i.p.)] across various experimental groups. Cognitive function was assessed using the passive avoidance test for long-term memory and two-trial Y-maze for spatial reference memory. Scopolamine (2 mg/kg, i.p.) was administered to induce memory impairment. The efficacy of EFA in mitigating scopolamine-induced cognitive deficits was evaluated, and memory maintenance was assessed over 6 weeks following treatment. Except for the EFA dose of 700 mg/kg which adversly affected passive avoidance test, its other doses had no significant impact on memory performance in scopolamine-free rats, as observed in both the passive avoidance test and the two-trial Y-maze; however, in rats with scopolamine-induced cognitive deficits, EFA (particularly at 70 mg/kg) significantly improved step-through latency in the passive avoidance test (P < 0.001). This suggests a dose-dependent reversal of memory impairment. In addition, EFA demonstrated sustained cognitive enhancement over a 6-week period without affecting body weight. The findings suggest that EFA has a protective effect against scopolamine-induced memory impairment and could serve as a potential therapeutic agent for neurodegenerative conditions associated with cognitive decline. Further research is required to elucidate the underlying mechanisms responsible for these effects. © 2025 Elsevier B.V., All rights reserved.