The purpose of this study was to evaluate the relationship of brain microvascular endothelial cell (BMECs) function and the exosomal miR-630 expression after subarachnoid hemorrhage (SAH). We evaluated the effects of blood cerebrospinal fluid (BCSF) on proliferation of BMECs by MTT at 0, 1, 3, 7 and 12 days and performed cell cycle analysis after BCSF treatment for 48 h. The expression of endothelial adhesion molecules (ICAM-1, VCAM-1 and ZO-1) were detected by qRT-PCR and immunofluorescent staining after BCSF treatment. NO produced by BMECs was also evaluated by Griess assay. The expression of exosomal miR-630 was analyzed by qRT-PCR in BCSF treated cell cultu normal cell culture medium andre medium. We further compared the exosomal miR-630 of clinical patients between aSAH and normal hydrocephalus. The adhesion molecules expression was further detected after co-incubation with exosomes transfected by miR-630 mimics. We found that BCSF significantly reduced the cell vitality in a time-dependent manner (p < 0.05) and the growth inhibition ratio reached 78.34 ± 9.22% on the 12th day. BCSF induced cell cycle arrest in G0/G1 phase in BMECs (p < 0.01). The expression of ICAM-1, VCAM-1, ZO-1 and the NO produced by BMECs were markedly reduced following incubation with BCSF. Then we demonstrated that the expression of exosomal miR-630 was markedly reduced in the BCSF treated BMECs and the same phenomenon occurred in aSAH patients compared with normal hydrocephalus. The expression of ICAM-1, VCAM-1 and ZO-1 were then increased in BMECs cocultured with exosomes transfected by miR-630 mimics. In conclusion, the low expression of exosomal miR-630 in CSF was closely related to endothelial function in BCSF endothelial cell injury model and clinical patients.