Prevention of inflammation is a mechanism of preconditioning-induced neuroprotection against focal cerebral ischemia
Prevention of inflammation is a mechanism of preconditioning-induced neuroprotection against focal cerebral ischemia
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DOI：
10.1016/j.neuint.2006.02.011
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发表时间：
2006-07-01
影响因子：
4.2
通讯作者：
Vemuganti, Raghu
中科院分区：
文献类型：
--
作者：
Bowen, Kellie K.;Naylor, Michelle;Vemuganti, Raghu
短暂的缺血性损伤诱导对随后的大面积缺血事件的显著保护。这种现象称为预处理（PC）诱导的缺血耐受的分子机制尚未完全了解。在中风后急性期观察到的炎症已知对神经学结果有害。我们目前评估PC的神经保护作用是否涉及预防缺血后炎症。成年大鼠队列进行短暂局灶性缺血（60分钟大脑中动脉闭塞; MCAO），PC（10分钟MCAO）和PC后72小时局灶性缺血。预先给予PC可显著降低缺血后许多炎性基因的表达，包括细胞因子、趋化因子、粘附分子和促炎性转录因子，并阻止中性粒细胞和巨噬细胞在局灶性缺血大鼠同侧皮质的浸润。PC还可减少短暂局灶性脑缺血引起的梗死体积和神经功能障碍。这些研究表明，预防炎症可能是PC诱导保护局灶性缺血的一种机制。(c)2006爱思唯尔有限公司保留所有权利。
A brief ischemic insult induces significant protection against subsequent massive ischemic events. The molecular mechanisms underlying this phenomenon known as preconditioning (PC)-induced ischemic tolerance are not completely understood. Inflammation seen during the acute phase after stroke is known to be detrimental to the neurological outcome. We presently evaluated if the neuroprotective actions of PC involves prevention of post-ischemic inflammation. Cohorts of adult rats were subjected to transient focal ischemia (60 min middle cerebral artery occlusion; MCAO), PC (10 min MCAO) and focal ischemia followed 72 h after PC. Prior PC significantly reduced the post-ischemic increased expression of many inflammatory genes including cytokines, chemokines, adhesion molecules and pro-inflammatory transcription factors, and prevented the infiltration of neutrophils and macrophages in the ipsilateral cortex of rats subjected to focal ischemia. PC also decreased the volume of infarction and neurological dysfunction caused by transient focal ischemia. These studies indicate that prevention of inflammation might be a contributing mechanism by which PC induces protection against focal ischemia. (c) 2006 Elsevier Ltd. All rights reserved.