Abstract： The pathophysiological mechanisms of subarachnoid hemorrhage (SAH) include early brain injury (EBI) and delayed cerebral ischemia. In recent years, researches have mainly focused on EBI. After blood enters the subarachnoid space, it can cause neuronal apoptosis, blood-brain barrier disruption, brain edema and neuroinflammation. Red blood cells and their metabolites activate resident immune cells in central nervous system and recruit peripheral inflammatory cells tinto the subarachnoid space, inducing neuroinflammation. The latter plays an important role in EBI and has a significant impact on the outcome of patients with SAH. This article reviews the role of neuroinflammation in EBI after SAH.