论文部分内容阅读
近年来对重要的炎症信号分子启动及促进缺血后炎症反应作用的研究取得了许多进展,如NF-κB对前炎症基因的表达和调控有协调作用;黏附分子在脑缺血区域水平上调;缺血诱导NO生成增多而加重缺血损伤;选择性COX-2抑制剂则能减少梗死体积;炎症因子在脑缺血中起损伤-修复双重效应等。抑制缺血后炎症反应成为减少脑缺血后损伤的新的治疗策略。我们将最近的这些研究进展进行综述,以提高我们对缺血后炎症反应在缺血性卒中作用的认识。
In recent years, many important progresses have been made in the initiation of important inflammatory signaling molecules and in the promotion of postischemic inflammatory response. For example, NF-κB has a coordinative effect on the expression and regulation of pro-inflammatory genes; the adhesion molecules are upregulated in ischemic areas; Ischemia induces increased NO production and aggravates ischemic injury; selective COX-2 inhibitors reduce infarct volume; inflammatory factors play a role in cerebral ischemia - repairing dual effects. Inhibition of post-ischemic inflammation becomes a new therapeutic strategy to reduce post-ischemic damage. We review these recent advances in research to improve our understanding of the role of postischemic inflammatory responses in ischemic stroke.