Glutathione monoethyl ester provides neuroprotection in a rat model of stroke

被引:65
作者
Anderson, MF
Nilsson, M
Eriksson, PS
Sims, NR
机构
[1] Sahlgrens Univ Hosp, Inst Clin Neurosci, S-41345 Gothenburg, Sweden
[2] Flinders Univ S Australia, Sch Med, Dept Med Biochem, Adelaide, SA 5001, Australia
[3] Flinders Univ S Australia, Flinders Med Res Inst, Ctr Neurosci, Adelaide, SA 5001, Australia
基金
英国医学研究理事会;
关键词
focal ischaemia; rats; oxidative stress; infarction; glutathione ester; stroke;
D O I
10.1016/j.neulet.2003.09.067
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Oxidative stress plays an important role in the development of tissue damage following transient focal cerebral ischaemia. Glutathione is a central component in the antioxidant defence of cells. We have previously shown a close association between mitochondrial glutathione loss and cell death following middle cerebral artery (MCA) occlusion. Glutathione monoethyl ester increases cellular glutathione and is particularly effective in increasing the mitochondrial pool. In the present investigation, we infused glutathione monoethyl ester into the third ventricle during 2 h of MCA occlusion and 48 h of reperfusion. Infarct size was reduced from 46% of the total ischaemic hemisphere in saline-treated animals to 16% following ester treatment. Thus, glutathione monoethyl ester provides neuroprotection following transient focal cerebral ischaemia. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:163 / 165
页数:3
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