Cerebral ischemia and inflammation
Cerebral ischemia and inflammation
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DOI：
10.1097/00019052-200102000-00014
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发表时间：
2001-02-01
影响因子：
4.8
通讯作者：
Alexander, M
中科院分区：
文献类型：
--
作者：
Iadecola, C;Alexander, M
脑缺血伴随着明显的炎症反应，该反应是由缺血诱导的细胞因子、粘附分子和其他炎症介质（包括前列腺素和一氧化氮）的表达引发的。临床前研究表明，旨在减轻此类炎症的干预措施可以减少脑缺血晚期发生的脑损伤的进展。特别是，阻断炎症相关酶（例如诱导型一氧化氮合酶和环氧合酶-2）活性的策略可以通过延长治疗窗来减少缺血性损伤。尽管使用抗细胞间粘附分子-1的鼠抗体的临床试验并未显示出对缺血性中风患者的益处，但最近的数据表明，异源蛋白诱导的免疫激活可能在该试验的失败中发挥了重要作用。因此，继续探索抗炎疗法在治疗晚期脑缺血中的功效是有充分理由的，Curr Opin Neurol 14:89-94。 （三）。 2001 年利平科特威廉姆斯和威尔金斯。
Cerebral ischemia is accompanied by a marked inflammatory reaction that is initiated by ischemia-induced expression of cytokines, adhesion molecules, and other inflammatory mediators, including prostanoids and nitric oxide. Preclinical studies suggest that interventions that are aimed at attenuating such inflammation reduce the progression of brain damage that occurs during the late stages of cerebral ischemia. In particular, strategies that block the activity of inflammation-related enzymes, such as inducible nitric oxide synthase and cyclooxygenase-2, reduce ischemic damage with an extended therapeutic window. Although a clinical trial using murine antibodies against intercellular adhesion molecule-1 did not show benefit in patients with ischemic stroke, recent data indicate that immune activation induced by the heterologous protein may have played an important role in the failure of this trial. Therefore, there is a strong rationale for continuing to explore the efficacy of anti-inflammatory therapies in the treatment of the late stages of cerebral ischemia, Curr Opin Neurol 14:89-94. (C). 2001 Lippincott Williams & Wilkins.