Anderson Michelle F, Nilsson Michael, Eriksson Peter S, Sims Neil R
Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden.
Neurosci Lett. 2004 Jan 9;354(2):163-5. doi: 10.1016/j.neulet.2003.09.067.
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.
氧化应激在短暂性局灶性脑缺血后组织损伤的发展中起重要作用。谷胱甘肽是细胞抗氧化防御的核心成分。我们之前已经表明，大脑中动脉（MCA）闭塞后线粒体谷胱甘肽的丧失与细胞死亡密切相关。谷胱甘肽单乙酯可增加细胞内谷胱甘肽，尤其在增加线粒体池方面效果显著。在本研究中，我们在MCA闭塞2小时和再灌注48小时期间将谷胱甘肽单乙酯注入第三脑室。梗死面积从盐水处理动物的缺血半球总面积的46%减少到酯处理后的16%。因此，谷胱甘肽单乙酯在短暂性局灶性脑缺血后提供神经保护作用。
