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.

译文

我们先前的研究表明,在大鼠短暂性大脑中动脉闭塞模型中,再灌注2小时后,阿魏酸 (4-羟基-3-甲氧基肉桂酸,FA) 抑制缺血纹状体中细胞间粘附分子-1 (ICAM-1) 的表达。目的进一步探讨FA在脑缺血再灌注过程中的神经保护作用。大鼠缺血90分钟; 然后在再灌注2、10、24和36小时后处死它们。在再灌注2 h时,使用半定量rt-pcr检测ICAM-1和巨噬细胞-1抗原 (Mac-1) mRNA。在2时测量Mac-1,4-羟基-2-壬醛 (4-HNE),8-羟基-2 '-脱氧鸟苷 (8-OHdG),活性半胱天冬酶3,神经元核 (NeuN) 和TUNEL阳性细胞,再灌注10、24和36小时。FA (100 mg/kg,i.v.) 后立即给予MCAo抑制了再灌注2 h时纹状体中ICAM-1和Mac-1 mRNA的表达,并减少了Mac-1,4-hne和8-OHdG阳性细胞的数量。缺血边缘和核心在10,再灌注24和36 h。FA在再灌注10 h时减少半影中的TUNEL阳性细胞,在再灌注24和36 h时减少缺血边界和核心中的TUNEL阳性细胞。FA在10小时减少了半影中的caspase 3活性表达,并在再灌注36小时恢复了半影和缺血核心中的NeuN标记神经元。FA降低了ICAM-1 mRNA的水平和小胶质细胞/巨噬细胞的数量,随后下调了炎症诱导的氧化应激和氧化应激相关的凋亡,提示FA通过抑制大鼠脑缺血/再灌注损伤后ICAM-1 mRNA的表达来提供针对氧化应激相关凋亡的神经保护。

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