Liao Su-Lan, Chen Wen-Yin, Raung Shue-Ling, Chen Chun-Jung
Department of Education and Research, Taichung Veterans General Hospital, No. 160, Sec. 3, Taichung-Gang Rd, Taichung 407, Taiwan, PR China.
Neuroreport. 2003 Nov 14;14(16):2089-94. doi: 10.1097/00001756-200311140-00016.
Reactive oxygen species play a critical role in ischemic injury and oxidative stress induces apoptosis and triggers inflammation in neural cells. The effect of ethanol on ischemic brain injury was examined. Ethanol attenuated ischemia/reperfusion-induced brain infarction and elevation of inflammatory mediators, including tumor necrosis factor-alpha (TNF-alpha) expression, metalloproteinase-9, and neutrophil-associated myeloperoxidase activities. In cultured neurons, ethanol suppressed combined oxygen and glucose deprivation (COGD)/reoxygenation-induced oxidative stress and neuronal apoptosis. Furthermore, ethanol suppressed COGD/reoxygenation-induced activation of NF-kappaB, a free-radical-sensitive regulator, leading to the attenuation of TNF-alpha expression in glial cultures. We propose that scavenging of free radicals and attenuation of free-radical-induced alterations might account for ethanol's beneficial action against ischemic brain injury.
活性氧在缺血性损伤中起关键作用，氧化应激诱导神经细胞凋亡并引发炎症。研究了乙醇对缺血性脑损伤的影响。乙醇减轻了缺血/再灌注诱导的脑梗死以及炎症介质的升高，包括肿瘤坏死因子-α（TNF-α）表达、金属蛋白酶-9和中性粒细胞相关髓过氧化物酶活性。在培养的神经元中，乙醇抑制了联合氧糖剥夺（COGD）/复氧诱导的氧化应激和神经元凋亡。此外，乙醇抑制了COGD/复氧诱导的NF-κB激活，NF-κB是一种对自由基敏感的调节因子，导致胶质细胞培养中TNF-α表达的减弱。我们认为清除自由基和减轻自由基诱导的改变可能是乙醇对缺血性脑损伤有益作用的原因。
