Ameliorative effect of rosmarinic acid on scopolamine-induced memory impairment in rats

• Published in: Neuroscience letters Vol. 585; pp. 23 - 27
• Main Authors: Hasanein, Parisa, Mahtaj, Azam Kazemian
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 12.01.2015
• Subjects: Animals; Avoidance Learning - drug effects; Cholinergic Antagonists; Cinnamates - pharmacology; Cinnamates - therapeutic use; Depsides - pharmacology; Depsides - therapeutic use; Donepezil; Indans - pharmacology; Learning; Male; Memory; Memory - drug effects; Memory Disorders - chemically induced; Memory Disorders - drug therapy; Memory Disorders - psychology; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Piperidines - pharmacology; Rats; Rats, Wistar; Reaction Time - drug effects; Rosmarinic Acid; Scopolamine; Learning; Rats; Rosmarinic acid; Scopolamine; Memory; Donepezil
• ISSN: 0304-3940; 1872-7972; 1872-7972
• DOI: 10.1016/j.neulet.2014.11.027

•RA administration (16 and 32mg/kg) improved learning and memory in control rats.•RA (8mg/kg) did not alter cognitive function in sopolamine treated rats.•RA 16 and 32mg/kg treated rats had longer STLr in memory deficit groups.•Higher doses of RA caused increased TDC in scopolamine treated animals.•RA may protect against memory deficits in a pharmacological model of AD. Rosmarinic acid (RA) is a natural phenol that exerts different biological activities, such as antioxidant activity and neuroprotective effects. In this study, we hypothesized that administration of RA (8, 16, and 32mg/kg, p.o.) for 7 days would effect on scopolamine-induced cognitive dysfunction as an extensively used model of cognitive impairment. The rats were divided into 10 groups. The acquisition trial was done 1h after the last administration of RA. Animals were divided into control, RA (8, 16, and 32mg/kg) and donepezil (2mg/kg) treated controls, scopolamine, RA (8, 16, and 32mg/kg), and donepezil (2mg/kg) treated scopolamine groups. Memory impairment was induced by scopolamine treatment (1mg/kg, i.p.) 30min after the administration of RA, donepezil, or saline. Scopolamine administration caused cognition deficits in the PAL and memory paradigm. While orally RA administration (16 and 32mg/kg) improved learning and memory in control rats, it reversed learning and memory deficits of scopolamine received groups. Administration of RA at the dose of 8mg/kg did not alter cognitive function in control and scopolamine treated groups. The combination of anticholinesterase, neuroprotective, and antioxidant properties of RA may all be responsible for the observed effects. These results indicate the beneficial effects of subchronic RA administration in passive avoidance learning and memory in control rats as well as in a pharmacological model of cholinergic deficit which continue to expand the knowledge base in creating new treatment strategies for cognition deficits and dementia. Of course, further studies are warranted for clinical use of RA in the management of demented subjects.