Objective To study the protective mechanism of astaxanthin against early brain injury (EBI) after subarachnoid hemorrhage (SAH) in mice.Methods Male ICR mice were randomly divided into SAH group, sham operation group, SAH+vehicle (DMSO) group, and SAH+astaxanthin group. A SAH model was established by injecting fresh blood into the prechiasmatic cistern. At 24 hours after surgery, neurological function was scored; the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling method and Western blot were used to measure the content of NOX2 protein in brain tissue; enzyme-linked immunosorbent assay was used to determine the level of TNF-a/IL-1β; the water content in brain tissue was evaluated by the wet-dry weight method.Results Compared with the control group, the SAH group had a higher score for neurological impairment, more severe cerebral edema, a significantly higher level of NOX2 protein and a significantly larger number of apoptosis-positive cells in brain tissue, and a significantly higher level of TNF-a/IL-1β. In mice treated with astaxanthin, neurological function was improved, and the apoptosis-positive cells in brain tissue were significantly reduced. At the same time, astaxanthin reduced the level of NOX2 protein in brain tissue and the level of TNF-a/IL-1β after SAH.Conclusions Astaxanthin has a protective effect against EBI after SAH, probably by its antioxidant capacity.