Reduction of cerebral infarction in rats by biliverdin associated with amelioration of oxidative stress
Reduction of cerebral infarction in rats by biliverdin associated with amelioration of oxidative stress
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DOI：
10.1016/j.brainres.2007.07.104
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发表时间：
2008-01-10
期刊：
影响因子：
2.9
通讯作者：
Abe, Koji
中科院分区：
文献类型：
--
作者：
Deguchi, Kentaro;Hayashi, Takeshi;Abe, Koji
胆绿素（BV）是血红素加氧酶（HO）系统催化血红素的副产物之一，是活性氧（ROS）的清除剂。我们假设BV治疗可以通过其抗氧化功效保护大鼠脑细胞免受氧化损伤。采用短暂性大脑中动脉闭塞（tMCAO）90 min，再灌注法制备脑梗死模型。再灌注后立即腹腔内给予BV或载体。采用氯化三苯基四氮唑（TTC）染色法观察tMCAO后2天脑梗死面积的变化。tMCAO后4小时的超氧化物生成通过检测氧化的氢乙啶来确定。此外，通过4-羟基-2-壬烯醛（4-HNE）脂质过氧化染色和8-羟基-2 '-脱氧鸟苷（8-OHdG）DNA损伤的化学方法评估神经元的氧化损伤。BV治疗显著减少了脑皮质的梗死体积，减少了超氧化物的产生，减少了脑细胞的氧化损伤。本研究表明，BV治疗可减轻大鼠tMCAO模型神经元的氧化损伤，减少脑梗死面积。(c)2007 Elsevier B. V.保留所有权利。
Biliverdin (BV), one of the byproducts of heme catalysis through heme oxygenase (HO) system, is a scavenger of reactive oxygen species (ROS). We hypothesized that BV treatment could protect rat brain cells from oxidative injuries via its anti-oxidant efficacies. Cerebral infarction was induced by transient middle cerebral artery occlusion (tMCAO) for 90 min, followed by reperfusion. BV or vehicle was administered intraperitoneally immediately after reperfusion. The size of the cerebral infarction 2 days after tMCAO was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) stain. Superoxide generation 4 h after tMCAO was determined by detection of oxidized hydroethidine. In addition, the oxidative impairment of neurons were immunohistochemically assessed by stain for lipid peroxidation with 4-hydroxy-2-nonenal (4-HNE) and damaged DNA with 8-hydroxy-2'-deoxyguanosine (8-OHdG). BV treatment significantly reduced infarct volume of the cerebral cortices associated with less superoxide production and decreased oxidative injuries of brain cells. The present study demonstrated that treatment with BV ameliorated the oxidative injuries on neurons and decreased brain infarct size in rat tMCAO model. (c) 2007 Elsevier B.V. All rights reserved.