Interleukin‐18 mediated inflammatory brain injury after intracerebral hemorrhage in male mice

Abstract Interleukin‐18 (IL‐18), a pro‐inflammatory cytokine, is thought to be associated with inflammation in many neurological diseases such as ischemic stroke and poststroke depression, but the role of IL‐18 in inflammatory injury after intracerebral hemorrhage (ICH) remains unclear. In this study, we established the ICH model in male mice and found that IL‐18 expression including protein and mRNA levels was significantly increased in brain tissues after ICH. Meanwhile, exogenous IL‐18 exacerbated cerebral hematoma and neurological deficits following ICH. In the IL‐18 knockout group, the size of hematoma and neurological functions after ICH was decreased compared with the wild‐type group, suggesting the critical role of IL‐18 on the modulation of brain injury after ICH. Importantly, exogenous IL‐18 increased microglial activation in brain tissues after ICH. Furthermore, IL‐18 knockout resulted in the reduction of activated microglia after ICH. These results indicated that IL‐18 may regulate the inflammatory response after ICH through the activation of microglia. Thus, IL‐18 is expected to be a promising therapeutic target for secondary brain injury after ICH.