Resveratrol protects against oxidative injury induced by H 2O 2 in acute hippocampal slice preparations from Wistar rats

Abstract

There is a current interest in dietary compounds (such as trans-resveratrol) that can inhibit or reverse oxidative stress, the common pathway for a variety of brain disorders, including Alzheimer’s disease and stroke. The objective of the present study was to investigate the effects of resveratrol, under conditions of oxidative stress induced by H 2O 2, on acute hippocampal slices from Wistar rats. Here, we evaluated cell viability, extracellular lactate, glutathione content, ERK MAPK activity, glutamate uptake and S100B secretion. Resveratrol did not change the decrease in lactate levels and in cell viability (by MTT assay) induced by 1 mM H 2O 2, but prevented the increase in cell permeability to Trypan blue induced by H 2O 2. Moreover, resveratrol per se increased total glutathione levels and prevented the decrease in glutathione induced by 1 mM H 2O 2. The reduction of S100B secretion induced by H 2O 2 was not changed by resveratrol. Glutamate uptake was decreased in the presence of 1 mM H 2O 2 and this effect was not prevented by resveratrol. There was also a significant activation of ERK1/2 by 1 mM H 2O 2 and resveratrol was able to completely prevent this activation, leading to activity values lower than control levels. The impairments in astrocyte activities, induced by H 2O 2, confirmed the importance of these cells as targets for therapeutic strategy in brain disorders involving oxidative stress. This study reinforces the protective role of resveratrol and indicates some possible molecular sites of activity of this compound on glial cells, in the acute damage of brain tissue during oxidative stress.