TY - JOUR
T1 - Resveratrol protects against oxidative injury induced by H2O2 in acute hippocampal slice preparations from Wistar rats
AU - de Almeida, Lúcia Maria Vieira
AU - Leite, Marina Concli
AU - Thomazi, Ana Paula
AU - Battu, Cíntia
AU - Nardin, Patrícia
AU - Tortorelli, Lucas Silva
AU - Zanotto, Caroline
AU - Posser, Thaís
AU - Wofchuk, Susana Tchernin
AU - Leal, Rodrigo Bainy
AU - Gonçalves, Carlos Alberto
AU - Gottfried, Carmem
N1 - Funding Information:
This work was supported by Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) and FINEP/ Rede IBN 01.06.0842-00.
PY - 2008/12/1
Y1 - 2008/12/1
N2 - 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 H2O2, on acute hippocampal slices from Wistar rats. Here, we evaluated cell viability, extracellular lactate, glutathione content, ERKMAPK 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 H2O2, but prevented the increase in cell permeability to Trypan blue induced by H2O2. Moreover, resveratrol per se increased total glutathione levels and prevented the decrease in glutathione induced by 1 mM H2O2. The reduction of S100B secretion induced by H2O2 was not changed by resveratrol. Glutamate uptake was decreased in the presence of 1 mM H2O2 and this effect was not prevented by resveratrol. There was also a significant activation of ERK1/2 by 1 mM H2O2 and resveratrol was able to completely prevent this activation, leading to activity values lower than control levels. The impairments in astrocyte activities, induced by H2O2, 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.
AB - 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 H2O2, on acute hippocampal slices from Wistar rats. Here, we evaluated cell viability, extracellular lactate, glutathione content, ERKMAPK 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 H2O2, but prevented the increase in cell permeability to Trypan blue induced by H2O2. Moreover, resveratrol per se increased total glutathione levels and prevented the decrease in glutathione induced by 1 mM H2O2. The reduction of S100B secretion induced by H2O2 was not changed by resveratrol. Glutamate uptake was decreased in the presence of 1 mM H2O2 and this effect was not prevented by resveratrol. There was also a significant activation of ERK1/2 by 1 mM H2O2 and resveratrol was able to completely prevent this activation, leading to activity values lower than control levels. The impairments in astrocyte activities, induced by H2O2, 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.
KW - Astrocyte
KW - Glutamate uptake
KW - Glutathione
KW - Resveratrol
KW - S100B protein
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U2 - 10.1016/j.abb.2008.09.006
DO - 10.1016/j.abb.2008.09.006
M3 - Article
C2 - 18835240
AN - SCOPUS:55549098882
VL - 480
SP - 27
EP - 32
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
SN - 0003-9861
IS - 1
ER -