• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Critical care : >Interferon-β attenuates lung inflammation following experimental subarachnoid hemorrhage
【24h】

Interferon-β attenuates lung inflammation following experimental subarachnoid hemorrhage

机译：实验性蛛网膜下腔出血后干扰素-β可减轻肺部炎症

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

IntroductionAneurysmal subarachnoid hemorrhage (SAH) affects relatively young people and carries a poor prognosis with a case fatality rate of 35%. One of the major systemic complications associated with SAH is acute lung injury (ALI) which occurs in up to one-third of the patients and is associated with poor outcome. ALI in SAH may be predisposed by neurogenic pulmonary edema (NPE) and inflammatory mediators. The objective of this study was to assess the immunomodulatory effects of interferon-β (IFN-β) on inflammatory mediators in the lung after experimental SAH.MethodsMale Wistar rats were subjected to the induction of SAH by means of the endovascular filament method. Sham-animals underwent sham-surgery. Rats received IFN-β for four consecutive days starting at two hours after SAH induction. After seven days, lungs were analyzed for the expression of inflammatory markers.ResultsSAH induced the influx of neutrophils into the lung, and enhanced expression of the pulmonary adhesion molecules E-selectin, inter-cellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 compared to sham-animals. In addition, SAH increased the expression of the chemokines macrophage inflammatory protein (MIP)-1α, MIP-2, and cytokine-induced neutrophil chemoattractant (CINC)-1 in the lung. Finally, tumor necrosis factor-α (TNF-α) was significantly increased in lungs from SAH-animals compared to sham-animals. IFN-β effectively abolished the SAH-induced expression of all pro-inflammatory mediators in the lung.ConclusionsIFN-β strongly reduces lung inflammation after experimental SAH and may therefore be an effective drug to prevent SAH-mediated lung injury.
机译：简介动脉瘤性蛛网膜下腔出血（SAH）影响相对年轻的人群，预后较差，病死率为35％。与SAH相关的主要系统性并发症之一是急性肺损伤（ALI），它发生在多达三分之一的患者中，并且与不良预后相关。 SAH中的ALI可能由神经源性肺水肿（NPE）和炎症介质引起。本研究的目的是评估实验性SAH后干扰素-β（IFN-β）对肺炎性介质的免疫调节作用。方法采用Wistar大鼠雄性Wistar大鼠血管内细丝法诱导SAH。假动物接受了假手术。从SAH诱导后两个小时开始，大鼠连续四天接受IFN-β。 7天后，分析肺中炎症标志物的表达。结果SAH诱导中性粒细胞流入肺，并增强肺黏附分子E-选择素，细胞间黏附分子（ICAM）-1和血管细胞的表达粘附分子（VCAM）-1与假动物相比。此外，SAH增加了趋化因子巨噬细胞炎症蛋白（MIP）-1α，MIP-2和细胞因子诱导的中性粒细胞趋化因子（CINC）-1在肺中的表达。最后，与假动物相比，SAH动物的肺部肿瘤坏死因子-α（TNF-α）显着增加。 IFN-β有效地消除了SAH诱导的肺中所有促炎介质的表达。结论IFN-β可以强烈减轻实验性SAH后的肺部炎症，因此可能是预防SAH介导的肺损伤的有效药物。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号