Increased oxidative stress during hyperglycemic cerebral ischemia
Increased oxidative stress during hyperglycemic cerebral ischemia
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DOI：
10.1016/j.neuint.2007.03.002
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发表时间：
2007-06-01
影响因子：
4.2
通讯作者：
Montgomery, Jane
中科院分区：
文献类型：
--
作者：
Bemeur, Chantal;Ste-Marie, Line;Montgomery, Jane
本文就高血糖在脑缺血中的作用作一综述。在实验和临床中风期间发生的高血压与脑损伤的增加有关。高血糖导致的氧化应激增加被认为是导致损伤加剧的原因。更具体地，超氧化物、一氧化氮和过氧亚硝酸盐被认为在脑损伤中起重要作用。这也涉及增加各种血细胞向缺血区的募集，这有助于炎症。我们目前的数据，从我们的小组和其他人证明，自由基的生产增加，在高血糖中风的啮齿动物。最近的数据表明，炎症是正常和高血糖条件下缺血性损伤的重要组成部分。我们总结了大量的研究表明，各种抗氧化剂（抑制自由基的产生，清除自由基和增加自由基降解）和抗炎策略减少脑梗死。最后，我们比较了这些策略在临床试验中的成功与动物模型。(C)2007爱思唯尔有限公司保留所有权利。
In this review, we summarize the role of hyperglycemia during cerebral ischemia. Hyperglycemia occurring during experimental and clinical stroke has been associated with increased cerebral damage. Increased oxidative stress resulting from hyperglycemia is believed to contribute to the exacerbated damage. More specifically, superoxide, nitric oxide and peroxynitrite are believed to play an important role in cerebral damage. This also involves increased recruitment of various blood cells to the ischemic zone that contribute to inflammation. We present data from our group and others that demonstrate that free radical production is increased during hyperglycemic stroke in rodents. Recent data suggest that inflammation is an important component of ischemic damage under both normo- and hyperglycemic conditions. We summarize numerous studies that indicate that a variety of antioxidant (inhibition of free radical production, scavenging of free radicals and increasing free radical degradation) and anti-inflammatory strategies decrease cerebral infarction. Finally, we compare the success of some of these strategies in clinical trials compared to the animal models. (C) 2007 Elsevier Ltd. All rights reserved.