Neuroproteção provida pelo extrato hidroalcoólico e frações de anacardium microcarpum–duke contra o dano induzido pelo peróxido de hidrogênio em fatias corticais de gallus gallus

Abstract

Studies focused on biological properties of different species of plants have shown some properties that help on treatment of several diseases, by obtaining active ingredients that have pharmacological and biotechnological properties. Oxidative stress is characterized by an increased production of reactive oxygen and nitrogen species, among then H2O2 which are involved in several neurodegenerative diseases. This fact has motivated the search for antioxidants therapies. Superior plants show high concentrations of many compounds with antioxidants potential in your composition. They also possess metabolites with a significant biotechnological potential. The goal of this study was to evaluate a possible neuroprotection provide by A. microcarpum hidroalcoholic extract (EHAM), A. microcarpum methanolic extract (EMAM) and A. microcarpum ethil acetate extract (EAAM) against oxidative stress induced by H2O2 in brain slices of little chicks (Gallus gallus), as well as the biochemical mechanisms involved in this effect. For this purpose, we used cortical micro slices obtained from little chicks (Gallus gallus) aging 5 – 15 days. The slices were incubated for 1 hour in oxygenated buffer HEPES-saline with or without H2O2 and different A. microcarpum fractions concentration (1-1000 μg/mL). After treatments, cellular viability was evaluated by the colorimetric method of MTT. Methanolic fraction showed better neuroprotective effect with relation to other two extracts and was used for further assays: lipid peroxidation (TBARS), total thiols (protein and non protein thiols) and ERK phosphorylation by Western Blot. Our results showed that EMAM and EHAM protected against cellular damage caused by H2O2 on 10 μg/mL and 1000 μg/mL respectively. The treatments didn’t cause any alteration on proteics and non proteics thiols. EMAM reversed to control levels the lipidic peroxidation induced by H2O2 from 100 μg/mL. MAPK involvement in this effect was also evaluated. ERK phosphorylation was stimulated when the slices were incubated with H2O2, and this effect wasn’t altered by the extract. Further experiments are necessary to understand the mechanism by which extracts provide neuroprotection.