Ferulic acid provides neuroprotection against oxidative stress-related apoptosis after cerebral ischemia/reperfusion injury by inhibiting ICAM-1 rnRNA expression in rats
Ferulic acid provides neuroprotection against oxidative stress-related apoptosis after cerebral ischemia/reperfusion injury by inhibiting ICAM-1 rnRNA expression in rats
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DOI：
10.1016/j.brainres.2008.02.090
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发表时间：
2008-05-13
期刊：
影响因子：
2.9
通讯作者：
Hsieh, Ching-Liang
中科院分区：
文献类型：
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作者：
Cheng, Chin-Yi;Su, Shan-Yu;Hsieh, Ching-Liang
我们以前的研究表明，阿魏酸（4-羟基-3-甲氧基肉桂酸，FA）抑制大鼠短暂性大脑中动脉闭塞模型再灌注2小时后缺血纹状体中细胞间粘附分子-1（ICAM-1）的表达。本研究的目的是进一步研究FA在脑缺血再灌注过程中的神经保护作用。大鼠进行90分钟的缺血，然后在2，10，24和36小时的再灌注后处死。半定量RT-PCR检测再灌注2 h时ICAM-1和Macrophage-1antigen（Mac-1）mRNA的表达。于再灌注2、10、24和36 h检测Mac-1、4-羟基-2-壬烯醛（4-HNE）、8-羟基-2 '-脱氧鸟苷（8-OHdG）、活性半胱氨酸蛋白酶3（caspase 3）、神经元核（NeuN）和TUNEL阳性细胞。FA（100 mg/kg，i.v.）MCAo后立即给药可抑制再灌注2 h纹状体ICAM-1和Mac-1 mRNA的表达，并减少再灌注10、24和36 h缺血边缘和核心区Mac-1、4-HNE和8-OHdG阳性细胞的数量。FA可使再灌注10 h缺血半暗带、24 h和36 h缺血边缘和核心区TUNEL阳性细胞减少。FA在10 h时减少半暗带中的活性caspase 3表达，并在再灌注36 h时恢复半暗带和缺血核心中的NeuN标记神经元。FA降低ICAM-1 mRNA水平和小胶质细胞/巨噬细胞数量，下调炎症诱导的氧化应激和氧化应激相关凋亡，提示FA通过抑制ICAM-1 mRNA表达对大鼠脑缺血再灌注损伤后氧化应激相关凋亡具有神经保护作用。(C)2008年由Elsevier B. V.出版。
our previous studies have shown that ferulic acid (4-hydroxy-3-methoxycinnamic acid, FA) inhibits intercellular adhesion molecule-1 (ICAM-1) expression in the ischemic striatum after 2 h of reperfusion in a transient middle cerebral artery occlusion model in rats. The purpose of this study is to further investigate the neuroprotective effects of FA during reperfusion after cerebral ischemia. Rats were subjected to 90 min of ischemia; they were then sacrificed after 2, 10, 24 and 36 h of reperfusion. ICAM-1 and macrophage-1 antigen (Mac-1) mRNA were detected using semi-quantitative RT-PCR at 2 h of reperfusion. Mac-1, 4-hydroxy-2-nonenal (4-HNE), 8-hydroxy-2'-deoxyguanosine (8-OHdG), active caspase 3, neuronal nuclei (NeuN) and TUNEL positive cells were measured at 2, 10, 24 and 36 h of reperfusion. FA (100 mg/kg, i.v.) administered immediately after MCAo inhibited ICAM-1 and Mac-1 mRNA expression in the striatum at 2 h of reperfusion, and reduced the number of Mac-1, 4-HNE and 8-OHdG positive cells in the ischemic rim and core at 10, 24 and 36 h of reperfusion. FA decreased TUNEL positive cells in the penumbra at 10 h, and in the ischemic boundary and core at 24 and 36 h of reperfusion. FA curtailed active caspase 3 expression in the penumbra at 10 h and restored NeuN-labeled neurons in the penumbra and ischemic core at 36 h of reperfusion. FA decreased the level of ICAM-1 mRNA and the number of microglia/macrophages, and subsequently down-regulated inflammation-induced oxidative stress and oxidative stress-related apoptosis, suggesting that FA provides neuroprotection against oxidative stress-related apoptosis by inhibiting ICAM-1 mRNA expression after cerebral ischemia/reperfusion injury in rats. (C) 2008 Published by Elsevier B.V.