• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Ischemic preconditioning-induced neuroprotection is associated with differential expression of IL-1beta and IL-1 receptor antagonist in the ischemic cortex.
【24h】

Ischemic preconditioning-induced neuroprotection is associated with differential expression of IL-1beta and IL-1 receptor antagonist in the ischemic cortex.

机译：缺血预处理诱导的神经保护作用与缺血皮层中IL-1beta和IL-1受体拮抗剂的差异表达有关。

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

Ischemic preconditioning (IP) is a phenomenon that organs develop a tolerance toward subsequent lethal ischemic insults. Among the factors that are involved in IP, IL-1beta and its endogenous receptor antagonist IL-1ra have been identified as important players in the induction of IP. The present study investigated whether IP affects the levels of these two antagonistic proteins during tolerance and reperfusion periods after ischemic stroke. The IP 24 h prior to ischemic stroke resulted in neuroprotection in the cortex. IP-induced protection is accompanied by increased IL-1beta gene and IL-1ra gene and protein levels during the tolerance period. In the post-ischemic cortex, IP resulted in the suppression of IL-1beta mRNA and protein levels at 6 h without affecting IL-1ra expression and the up-regulation of IL-1ra protein at 24 h. These findings demonstrate that IP differentially regulates cortical IL-1beta and IL-1ra expression before and after ischemic stroke and suggest that the shift toward an anti-inflammatory state in the post-ischemic cortex may contribute to IP-induced neuroprotection.
机译：缺血预处理（IP）是一种器官对随后的致命性缺血性损伤产生耐受性的现象。在涉及IP的因素中，IL-1β及其内源性受体拮抗剂IL-1ra被确定为诱导IP的重要参与者。本研究调查了IP是否会在缺血性中风后的耐受性和再灌注期间影响这两种拮抗蛋白的水平。缺血性中风之前的24小时IP可导致皮质神经保护。在耐受期内，IP诱导的保护伴随着IL-1beta基因和IL-1ra基因及蛋白质水平的升高。在缺血后皮质中，IP可在6 h抑制IL-1beta mRNA和蛋白水平，而不会影响IL-1ra表达和在24 h上调IL-1ra蛋白。这些发现表明，IP在缺血性中风之前和之后差异调节皮层IL-1beta和IL-1ra的表达，并提示缺血后皮层向抗炎状态的转变可能有助于IP诱导的神经保护。

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