Rosmarinic acid prevents against memory deficits in ischemic mice.

Autor: Fonteles AA; Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Fortaleza, Brazil; Institute of Biomedicine of Brazilian Semi-Arid, Fortaleza, Brazil., de Souza CM; Post-Graduate Programme in Medical Sciences, Department of Medicine, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil., de Sousa Neves JC; Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Fortaleza, Brazil., Menezes AP; Post-Graduate Programme in Medical Sciences, Department of Medicine, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil., Santos do Carmo MR; Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Fortaleza, Brazil., Fernandes FD; Post-Graduate Programme in Medical Sciences, Department of Medicine, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil., de Araújo PR; Post-Graduate Programme in Medical Sciences, Department of Medicine, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil., de Andrade GM; Post-Graduate Programme in Pharmacology, Department of Physiology and Pharmacology, Fortaleza, Brazil; Post-Graduate Programme in Medical Sciences, Department of Medicine, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil; Institute of Biomedicine of Brazilian Semi-Arid, Fortaleza, Brazil. Electronic address: gmatos@ufc.br.
Jazyk: angličtina
Zdroj: Behavioural brain research [Behav Brain Res] 2016 Jan 15; Vol. 297, pp. 91-103. Date of Electronic Publication: 2015 Oct 09.
DOI: 10.1016/j.bbr.2015.09.029
Abstrakt: Polyphenols have neuroprotective effects after brain ischemia. It has been demonstrated that rosmarinic acid (RA), a natural phenolic compound, possesses antioxidant and anti-inflammatory properties. To evaluate the effectiveness of RA against memory deficits induced by permanent middle cerebral artery occlusion (pMCAO) mice were treated with RA (0.1, 1, and 20mg/kg/day, i.p. before ischemia and during 5 days). Animals were evaluated for locomotor activity and working memory 72 h after pMCAO, and spatial and recognition memories 96 h after pMCAO. In addition, in another set of experiments brain infarction, neurological deficit score and myeloperoxidase (MPO) activity were evaluates 24h after the pMCAO. Finally, immunohistochemistry, and western blot, and ELISA assay were used to analyze glial fibrillary acidic protein (GFAP), and synaptophysin (SYP) expression, and BDNF level, respectively. The working, spatial, and recognition memory deficits were significantly improved with RA treatment (20mg/kg). RA reduced infarct size and neurological deficits caused by acute ischemia. The mechanism for RA neuroprotection involved, neuronal loss suppression, and increase of synaptophysin expression, and increase of BDNF. Furthermore, the increase of MPO activity and GFAP immunireactivity were prevented in MCAO group treated with RA. These results suggest that RA exerts memory protective effects probably due to synaptogenic activity and anti-inflammatory action.
(Copyright © 2015 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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