Mild hypothermia reduces ICAM-1 expression, neutrophil infiltration and microglia/monocyte accumulation following experimental stroke
Mild hypothermia reduces ICAM-1 expression, neutrophil infiltration and microglia/monocyte accumulation following experimental stroke
复制标题
DOI：
10.1016/s0306-4522(02)00350-0
复制
发表时间：
2002-01-01
期刊：
影响因子：
3.3
通讯作者：
Yenari, MA
中科院分区：
文献类型：
--
作者：
Wang, GJ;Deng, HY;Yenari, MA
亚低温是一种公认的抗脑缺血损伤的神经保护剂。研究表明，炎症增强脑缺血性损伤，特别是在再灌注的情况下。为了进一步阐明亚低温减弱炎症反应的机制，我们评估了内皮细胞间粘附分子-1（ICAM-1）的表达，中性粒细胞和单核细胞浸润，以及在常温和轻度低温条件下短暂局灶性脑缺血2小时后小胶质细胞的活化。在Sprague-Dawley大鼠中使用管腔内缝合方法诱导缺血。采用免疫组化法检测缺血后1、3、7天内皮细胞ICAM-1、浸润的中性粒细胞和单核细胞以及小胶质细胞。免疫阳性细胞和血管密度测定梗死周围区域。轻度低温与缺血后1天和3天的中性粒细胞减少，1天、3天和7天的ICAM-1阳性血管减少，3天和7天的单核细胞/活化小胶质细胞减少有关，但在第1天不相关。这些数据表明，轻度低温显着降低内皮细胞粘附分子的表达，急性（中性粒细胞）和亚急性（单核细胞）白细胞浸润，和小胶质细胞的激活，直到7天后，在啮齿动物模型的短暂局灶性脑缺血损伤。(C)2002年IBRO。由Elsevier Science Ltd.出版，版权所有。
Mild hypothermia is an established neuroprotectant against cerebral ischemic injury. Studies have shown that inflammation potentiates cerebral ischemic injury, particularly in the setting of reperfusion. To further elucidate the mechanism by which mild hypothermia attenuates the inflammatory response, we assessed endothelial intercellular adhesion molecule-1 (ICAM-1) expression, neutrophil and monocyte infiltration, and microglial activation following 2 h of transient focal cerebral ischemia under normothermic and mildly hypothermic conditions. Ischemia was induced using the intraluminal suture method in Sprague-Dawley rats. Immunohistochemistry was used to detect endothelial ICAM-1, infiltrating neutrophils and monocytes, and microglia at 1, 3, and 7 days post-ischemia. Immunopositive cell and vessel densities were measured in the peri-infarct region. Mild hypothermia was associated with decreased neutrophils at 1 and 3 days post-ischemia, decreased ICAM-1-positive vessels at 1, 3, and 7 days, and decreased monocytes/activated microglia at 3 and 7 days, but not at I day. These data demonstrate that mild hypothermia significantly reduces endothelial adhesion molecule expression, acute (neutrophil) and subacute (monocyte) leukocyte infiltration, and microglial activation up to 7 days following insult in a rodent model of transient focal cerebral ischemia. (C) 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved.