ArticleNeurochemical research2025
Anethole Ameliorates Scopolamine-Induced Memory Deficits and Neuronal Damage Through Antioxidant, Anti-Inflammatory, and Anticholinesterase Activities in Rats.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Zingerone mitigates cognitive and motor impairments in a D-galactose-induced brain aging model: Role of oxidative stress and neuroinflammation.Molecular biology reports · 2026Article
- Design, synthesis, and antifungal activity of anethole-based oxime ester compounds as potential laccase inhibitors.Pest management science · 2026Article
- The Role of Anethole in Reproductive Physiology and In Vitro Biotechnologies-A Review.Reproduction in domestic animals = Zuchthygiene · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Scopolamine-induced memory impairment is a well-established model for studying the therapeutic potential of novel compounds in the pathogenesis of Alzheimer's disease (AD). This study aimed to evaluate the protective effects and underlying mechanisms of anethole against scopolamine-induced memory and cognitive disorders. Rats were treated with scopolamine (0.7 mg/kg, i.p.) for 14 consecutive days. Anethole (125, 250, and 500 mg/kg, i.g.) was administered one hour prior to scopolamine injection. Memory and cognitive performance were assessed using the Passive Avoidance Test (PAT) and the Novel Object Recognition Test (NORT). In addition, blood-brain barrier (BBB) permeability, brain water content (BWC), and hippocampal levels of oxidative stress markers, inflammatory cytokines, acetylcholine (ACh), and acetylcholinesterase (AChE) were evaluated following the behavioral tests. Histological changes in the hippocampus were examined using hematoxylin and eosin (H&E) staining. Anethole treatment significantly improved scopolamine-induced memory deficits in both NORT and PAT. Furthermore, anethole reduced BBB permeability and BWC in the AD rat model. Hippocampal levels of oxidative stress and inflammation were also attenuated following anethole administration. Additionally, anethole exerted cholinergic effects by inhibiting AChE and increasing ACh levels in the scopolamine-induced AD model. The neuroprotective effects of anethole were further confirmed by H&E staining. Our findings demonstrate that anethole effectively reverses scopolamine-induced memory and cognitive impairments through antioxidant, anti-inflammatory, and anticholinesterase mechanisms in rats. Therefore, anethole may be considered a promising therapeutic candidate for alleviating symptoms of AD and warrants further investigation in future studies.
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Registered trials
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