Aims: In recent years, numerous studies demonstrated that Astragaloside Ⅳ(AST Ⅳ)has neuroprotective effects against cerebral ischemic-reperfusion injury, but whetherAstragalosideⅣattenuates early brain injury (EBI) after subarachnoid hemorrhage(SAH) is still not clear. In the present study, we aimed to determine the effect ofAstragalosideⅣon neurobehavior, cell apoptosis, oxidative stress injury and brainedema of EBI after experimental subarachnoid hemorrhage in rats. Methods: Rats (n=68) were randomly divided into the following groups: sham group,SAH group, SAH+saline (40 mg/kg) group, and SAH+AstragalosideⅣ(40 mg/kg)group. Astragaloside Ⅳ or an equal volume of physiological saline was administeredonce the day before SAH and at 1h and 6 h after SAH. Mortality,neurologicalscores, brain edema were assessed at 24 h after SAH, biochemical tests and histologi-cal studies were also performed at that point. Results: SAH induced an increase in the malondialdehyde (MDA) level, neuron apop-tosis, cleaved-caspase 3, brain edema and a decrease in neurobehavioral scores andactivities of Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Astra-galoside Ⅳ treatment reversed the changes. Conclusions: Our findings show that Astragaloside Ⅳ may alleviate EBI after SAHthrough antioxidation, inhibition of neuron apoptosis and reduction of brain edema.