Objective To investigate the effect of G protein-coupled receptor 30 （GPR30） on neuroinflammation and blood-brain barrier （BBB） disruption during early brain injury （EBI） in rats with subarachnoid hemorrhage （SAH）.Methods Thirty-six male rats were randomly divided into six groups （n = 6 per group）： sham operation （Sham） group and SAH （3 h， 6 h， 12 h， 24 h， 72 h） groups. In addition， 72 rats were randomly divided into four groups （n = 18 per group）： Sham group， SAH group， SAH combined with overexpressed GPR30 lentivirus negative vector （SAH+Lv-NC） group， SAH combined with overexpressed GPR30 lentivirus vector （SAH+Lv-GPR30） group. A Sprague-Dawley rat model of SAH was established by intravascular perforation. Intraventricular injection of Lv-GPR30 was performed in the rats with SHA. The effect of GPR30 on EBI was analyzed through neurological scoring， brain tissue water content measurement， Evans blue staining， and HE staining. The levels of proteins and their transcription levels were determined by Western blotting and real-time fluorescence quantitative PCR， respectively. ELISA was employed to measure the levels of tumor necrosis factor-alpha （TNF-α）， interleukin-6 （IL-6）， interleukin-1 beta （IL-1β）， and interleukin-10 （IL-10）.Results Intraventricular injection of Lv-GPR30 increased the expression of GPR30 in the brain tissue of rats with SAH and improved their neurological function， neuroinflammation， BBB disruption， and cerebral edema. Overexpression of GPR30 inhibited the expression of matrix metallopeptidase-9 and matrix metallopeptidase-2 as well as the inflammatory factors TNF-α， IL-6， and IL-1β in the brain tissue of SAH rats but increased the IL-10 level.Conclusions GPR30 can alleviate neuroinflammation and BBB disruption in rats with SAH.