Objective To investigate the effects of resveratrol on the neuroinflammation of brain tissue around hematoma after subarachnoid hemorrhage (SAH) and the underlying mechanisms.Methods Forty-eight adult male Sprague-Dawley rats were randomly divided into three groups:sham group, SAH group, and SAH+resveratrol group, with 16 rats in each group. A SAH model was constructed by double injection of blood into the cisterna magna. At 15 min before and 5 min after the model establishment, the SAH and SAH+resveratrol groups were treated with normal saline and resveratrol, respectively. At 72 h after SAH, we evaluated the neurological function of the rats using the neurological severity score, and then sacrificed them to obtain and preserve the brain tissue. ELISA was performed to determine the expression levels of proinflammatory cytokines (IL-1, IL-6, and TNF-α) and anti-inflammatory cytokines (IL-4, IL-10, and TGF-β). RT-PCR was used to measure the mRNA expression of M1 microglia markers (IL-1β and CD32) and M2 markers (CD206 and Arginase-1).Results Compared with the sham group, the SAH group had decreased neurological function (P<0.05), increased expression of the proinflammatory cytokines (IL-1, IL-6, and TNF-α) and anti-inflammatory cytokines (IL-4, IL-10, and TGF-β) in the brain tissue (P<0.05), and increased mRNA expression of the M1 markers (IL-1β and CD32) and M2 markers (CD206 and Arginase-1) (P<0.05). Compared with the SAH group, the SAH+resveratrol group showed significant reductions in neurological damage severity, the expression of the proinflammatory cytokines (IL-1, IL-6, and TNF-α), and the mRNA expression of the M1 markers (IL-1β and CD32) (P<0.05), and exhibited increases in the expression of the anti-inflammatory cytokines (IL-4, IL-10, and TGF-β) and the mRNA expression of the M2 markers (CD206 and Arginase-1) (P<0.05).Conclusions Resveratrol promotes a switch from M1 to M2 microglial phenotypes after SAH, and thereby alleviates neuroinflammation and neurological injury.