AVALIAÇÃO DO EFEITO PROFILÁTICO DA β-GLUCANA LASIODIPLODANA SOBRE MODELO DE NEUROINFLAMAÇÃO, DÉFICIT COGNITIVO E ESTRESSE OXIDATIVO EM RATOS

Abstract

Introduction: Alzheimer’s disease (AD) reaches 30 million people around the world. By the limited usage of the existent drugs to treat AD, that only relive the symptoms of it, several authors report the necessity of developing new compounds that are able to act in the early stages of AD, delaying it or, avoiding its appearance. Objective: Because of that, this study aims to analyze the prophylactic effect of a natural compound, (1-6)-β-D-glucan, lasiodiplodana, over an animal model of a chronic neuroinflammation. Methodology: 84 male wistar rats were allocated in 7 groups, being one receiving no treatment (CT) and the other receiving: saline (LPS-SAL and SAL-SAL) or 05, 10 and 15 mg/kg of lasiodiplodana (LPS-05mg, LPS-10mg, LPS-15mg and SAL-15mg). After 30 days of treatment, the animals received hippocamp injections of lipopolysaccharide – LPS (LPS-SAL, LPS-05mg, LPS-10mg and LPS-15mg) or saline (SAL-SAL e SAL-15mg). CT group did not pass through any surgical intervention. The locomotor/ exploratory and emotional activities were analyzed in open field and elevated plus mazes, respectively. In order to evaluate the memory of the animals, three tools were utilized: the open field maze with object recognition task, Morris water maze and the radial maze. After the behavioral tests, euthanasia was made and the brain of the rats were taken to later analyses of TBARs (thiobarbituric acid reactive substance) and nitrate/nitrite. Results: No significant difference was found in behavioral control tests among groups. In Morris water maze task, no group demonstrated significant results, but LPS-05mg group had a tendency to be different from LPS-SAL group. In the object recognition test no group showed significant results, however, LPS-10mg group had a tendency to be different from LPS-SAL group. The protocol utilized in radial maze was not efficient in evaluating the memory deficit of the rats from present study. In the analyses of TBARs and nitrate/nitrite the only group that was significantly (P<0.01) different from LPS-SAL was the one treated with 10 mg/kg of lasiodiplodana (LPS-10mg). Conclusion: It was concluded that the treatments with 05 mg/kg and 10mg/kg of lasiodiplodana were able to revert the memory deficit caused by the neuroinflammatory model, concerning associative and non-associative memories respectively, and the dosage of 10 mg/kg was capable of relieving the oxidative stress condition triggered by neuroinflammation.