...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Brain research >Social interaction modulates the neuroinflammatory response to global cerebral ischemia in male mice
【24h】

Social interaction modulates the neuroinflammatory response to global cerebral ischemia in male mice

机译：社交互动调节对雄性小鼠的全球脑缺血的神经炎性反应

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Social isolation is a risk factor for cardiovascular and cerebrovascular diseases, although the underlying mechanisms remain underspecified. Considering the potential of microglia to become sensitized by stressors and their role in neuroinflammation, we hypothesized that social isolation primes microglia, resulting in an exaggerated neuroimmune response to experimental cerebral ischemia. First, major histocompatibility complex II (MHC II) gene expression, an indicator of microglial priming, was compared between mice that were socially isolated or pair-housed. MHC II increased in the hippocampus and cortex of socially isolated mice, which is suggestive of isolation-induced microglial priming. In experiment 2, isolated and pair-housed mice underwent similar to 8 min of global cerebral ischemia. Hippocampal mRNA expression of tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) was significantly increased among both isolated and pair-housed ischemia groups relative to sham controls. Hippocampal expression of interleukin 1 beta (IL-1 beta and cortical INF-alpha, IL-1 beta and IL-6, were significantly increased 24-h postischemia in isolated mice, but not pair-housed mice, relative to controls. Ischemia-induced increases in microglial cell body area and percent area fraction of ionized calcium binding adaptor molecule 1 (Iba-1) positive staining were also observed in isolated, but not pair-housed mice, relative to controls. For experiment 3, brain sections from socially isolated and pair-housed mice underwent 15 min of oxygen glucose deprivation (OGD), an ex vivo model of cerebral ischemia. IL-6 gene expression was significantly elevated following OGD only in hippocampi from mice that had been socially isolated, indicating that isolation prior to ischemia is sufficient to modulate the neuroinflammatory response. Together, these data suggest microglial priming as a possible mechanism underlying the detrimental effects of social isolation on cerebral ischemia outcome. (C) 2017 Elsevier B.V. All rights reserved.
机译：社会隔离是心血管和脑血管疾病的危险因素，尽管潜在的机制仍然没有规定。考虑到微胶质细胞的潜力受到压力源的敏感性及其在神经炎症中的作用，我们假设社会隔离素质微胶质细胞，导致对实验性脑缺血的夸大神经影响反应。首先，在社会分离或配对的小鼠之间比较主要组织相容性综合体II（MHC II）基因表达，是微胶质灌注的指标。 MHC II在海马和社会上孤立的小鼠的皮质中增加，这是一种暗示分离诱导的微胶质灌注。在实验2中，分离和配对的小鼠接受了类似于全球脑缺血的8分钟。肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）的海马mRNA表达在相对于假对照的分离和配对的缺血基团中显着增加。白细胞介素1β（IL-1β和皮质INF-α，IL-1β和IL-6的海马表达明显增加了24小时后小鼠，但相对于对照组，而不是配对的小鼠。缺血 - 诱导的微胶质细胞体积和离子化钙结合衔接子分子1（IBA-1）的百分比百分比的增加，相对于对照，在分离，但不配对的小鼠中也观察到阳性染色。对于实验3，来自社会的脑部被隔离的和配对的小鼠接受了15分钟的氧葡萄糖剥夺（OGD），脑缺血的前体内模型。IL-6基因表达仅在来自社会分离的小鼠的小鼠中显着升高，表明在之前的分离缺血足以调节神经炎性反应。这些数据表明，微胶质灌注作为可能的机制，因为社会隔离对脑缺血结果的不利影响。 （c）2017 Elsevier B.v.保留所有权利。

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