Autophagy is a self-degradative process and it plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles and eliminating intracellular pathogens.Previous studies have demonstrated that autophagy pathway was activated in brain after experimental subarachnoid hemorrhage ( SAH),however the role of autophagy in the pathogenesis of early brain injury (EBI) following SAH remains unknown.Experiment 1 aimed to investigate the timecourse of the autophagy in the cortex following SAH.In experiment 2,we chose the maximum time pointof autophagy activation and assessed the effects of rapamycin (RAP,autophagy activator) and 3-Methyladenine (3-MA,autophagy inhibitor) on regulation of EBI.All SAH animals were subjected to injection of 0.3 ml fresh arterial,non-heparinized blood into prechiasmatic cistern in 20 seconds. As a result, Microtubule-associated protein light chain-3 (LC3), a biomarker of autophagosome,and beclin-1,a Bcl-2-interacting protein required for autophagy,were significantly increased at the early stage of SAH and their expressions peaked at 24 h after SAH.In RAP treated group,the early brain damage such as brain edema,blood-brain barrier (BBB) impairment,and clinical behavior scale was significantly ameliorated in compare with vehicle treated SAH rats.Conversely,3-MA decreased expression of LC3 and beclin-1,increased the average value of brain edema and BBB disfunction,and aggravated neurological deficits.Our results suggest that autophagy pathway is activated in the brain after SAH and may play a beneficial role to EBI development.