Hypoxia and ischemia are the main underlying pathogenesis of stroke and other neurological disorders. Cerebral hypoxia and/or ischemia (e.g., stroke) can lead to neuronal injury/death and eventually cause serious neurological disorders or even death in the patients. Despite knowing these serious consequences, there are limited neuroprotective strategies against hypoxic and ischemic insults in clinical settings. Recent studies indicate that microRNAs (miRNAs) are of great importance in regulating cerebral responses to hypoxic/ischemic stress in addition to the neuroprotective effect of the δ-opioid receptor (DOR). Moreover, new discovery shows that DOR can regulate miRNA expression and inhibit inflammatory responses to hypoxia/ischemia. We, therefore, summarize available data in current literature regarding the role of DOR and miRNAs in regulating the neuroinflammatory responses in this article. In particular, we focus on microglia activation, cytokine production, and the relevant signaling pathways triggered by cerebral hypoxia/ischemia. The intent of this review article is to provide a novel clue for developing new strategies against neuroinflammatory injury resulting from cerebral hypoxia/ischemia.

缺氧和缺血是中风和其他神经系统疾病的主要潜在发病机理。脑缺氧和/或缺血（例如中风）会导致神经元损伤/死亡，并最终导致患者严重的神经系统疾病甚至死亡。尽管知道这些严重后果，但在临床环境中针对缺氧和缺血性损伤的神经保护策略仍然有限。最近的研究表明，除了δ阿片受体（DOR）的神经保护作用外，microRNA（miRNA）在调节大脑对缺氧/缺血性应激的反应中也非常重要。此外，新发现表明DOR可以调节miRNA的表达并抑制对缺氧/缺血的炎症反应。因此，我们 本文总结了有关DOR和miRNA在调节神经炎症反应中的作用的现有文献中的可用数据。特别是，我们专注于小胶质细胞的激活，细胞因子的产生，以及由脑缺氧/缺血触发的相关信号通路。本文的目的是为开发针对脑缺氧/缺血引起的神经炎性损伤的新策略提供新线索。