Cerebral ischemia represents a major cause of disability, yet its precise mechanism remains unknown. In addition, ischemia-reperfusion injury which occurs during the blood recovery process increases the risk of mortality, and is not adequately addressed with current treatment. To improve therapeutic options, it is important to explore the vital substances that play a pivotal role in ischemia-reperfusion injury. This study is the first to investigate the role of IL-32, a vital pro-inflammatory factor, in models of cerebral ischemia-reperfusion injury. The results showed that IL-32 was highly expressed in both in vivo and in vitro models. The proteins of the NOD/MAPK/NF-κB pathway were also up-regulated, indicating a potential signaling pathway mechanism. Inhibition of IL-32 and blocking of the NOD/MAPK/NF-κB pathway increased cell survival, decreased the level of inflammatory factors and inflammasomes, and attenuated nitrosative stress. Taken together, the results show that inhibition of IL-32 expression ameliorates cerebral ischemia-reperfusion injury via the NOD/MAPK/NF-κB signaling pathway. The findings in this study reveal that IL-32 is a vital target of ischemia-reperfusion injury, providing a new avenue for treatment development.

脑缺血是导致残疾的主要原因，但其确切机制仍不清楚。此外，在血液恢复过程中发生的缺血再灌注损伤增加了死亡的风险，目前的治疗并未充分解决。为了改善治疗选择，重要的是探索在缺血再灌注损伤中起关键作用的重要物质。本研究首次研究了 IL-32（一种重要的促炎因子）在脑缺血再灌注损伤模型中的作用。结果显示IL-32在体内和体外模型中均高表达。NOD/MAPK/NF-κB通路的蛋白也上调，表明潜在的信号通路机制。抑制 IL-32 和阻断 NOD/MAPK/NF-κB 通路可增加细胞存活率，降低炎症因子和炎症小体的水平，减轻亚硝化应激。总之，结果表明，抑制 IL-32 表达可通过 NOD/MAPK/NF-κB 信号通路改善脑缺血再灌注损伤。本研究结果表明，IL-32 是缺血再灌注损伤的重要靶点，为治疗发展提供了新途径。