Resveratrol protects against oxidative injury induced by H₂O₂ in acute hippocampal slice preparations from Wistar rats

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• 作者：Lú ; cia Maria Vieira de Almeida ; Marina Concli Leite ; Ana Paula Thomazi ; Cí ; ntia Battu ; Patrí ; cia Nardin ; Lucas Silva Tortorelli ; Caroline Zanotto ; Thaí ; s Posser ; Susana Tchernin Wofchu
• 关键词：Astrocyte ; Glutamate uptake ; Glutathione ; Resveratrol ; S100B protein
• 刊名：Archives of Biochemistry and Biophysics
• 出版年：2008
• 出版时间：1 December 2008
• 年：2008
• 卷：480
• 期：1
• 页码：27-32
• 全文大小：371 K

文摘

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, 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 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.