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Abstract Title:

Tannic Acid Ameliorates STZ-Induced Alzheimer's Disease-Like Impairment of Memory, Neuroinflammation, Neuronal Death and Modulates Akt Expression.

Abstract Source:

Neurotox Res. 2020 Jan 29. Epub 2020 Jan 29. PMID: 31997154

Abstract Author(s):

Mariana F B Gerzson, Natália P Bona, Mayara S P Soares, Fernanda C Teixeira, Francine L Rahmeier, Fabiano B Carvalho, Marilda da Cruz Fernandes, Giovana Onzi, Guido Lenz, Relber A Gonçales, Roselia M Spanevello, Francieli M Stefanello

Article Affiliation:

Mariana F B Gerzson

Abstract:

Tannic acid (TA) is a hydrolysable glycosidic polyphenol polymer of gallic acid, which possesses neuroprotective properties. The aim of this study was to evaluate the effect of TA treatment on cognitive performance and neurochemical changes in an experimental model of sporadic dementia of Alzheimer's type (SDAT) induced by intracerebroventricular (ICV) injection of streptozotocin (STZ) and to explore the potential cellular and molecular mechanisms underlying these effects. Adult male rats were divided into four groups: control, TA, STZ, and TA + STZ. Animals from TA and TA + STZ groups were treated with TA (30 mg/kg) daily, by gavage, for 21 days; others groups received water (1 mL/kg). Subsequently, an ICV injection of STZ (3 mg/kg) was administered into the lateral ventricles of animals from STZ and TA + STZ groups, while other groups received citrate buffer. Cognitive deficits (short-term memory), neuronal survival, neuroinflammation as well as expression of SNAP-25, Akt, and pAkt were evaluated in the cerebral cortex. TA treatment protected against the impairment of memory in STZ-induced SDAT. STZ promoted an increase in neuronal death and the levels of proinflammatory cytokines (IL-6 and TNF-α) and a decrease in Akt and pAkt expression; TA was able to restore these changes. Neither STZ nor TA altered SNAP-25 expression or the levels of IL-12 and IL-4 in the cerebral cortex. Our study highlights that treatment with TA prevents memory deficits and reestablishes Akt and pAkt expression, protecting against neuronal death and neuroinflammation in STZ-induced SDAT in rats.

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