Bémeur Chantal, Ste-Marie Line, Montgomery Jane
Unité de Recherche en Sciences Neurologiques, PEA A-402, Centre de recherche du CHUM, Hôpital St-Luc, 1058 St-Denis, Montréal, Québec, Canada H2X 3J4.
Neurochem Int. 2007 Jun;50(7-8):890-904. doi: 10.1016/j.neuint.2007.03.002. Epub 2007 Mar 14.
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.
在本综述中,我们总结了高血糖在脑缺血过程中的作用。实验性和临床中风期间出现的高血糖与脑损伤增加有关。高血糖导致的氧化应激增加被认为是造成损伤加剧的原因。更具体地说,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。这还涉及各种血细胞向缺血区的募集增加,从而导致炎症。我们展示了我们团队及其他团队的数据,这些数据表明在啮齿动物的高血糖性中风期间自由基产生增加。最近的数据表明,在正常血糖和高血糖条件下,炎症都是缺血性损伤的重要组成部分。我们总结了大量研究,这些研究表明各种抗氧化策略(抑制自由基产生、清除自由基和增加自由基降解)和抗炎策略可减少脑梗死。最后,我们比较了其中一些策略在临床试验与动物模型中的成功情况。