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The role of vascular endothelial growth factor(VEGF)in early brain injury(EBI)after subarachnoid hemorrhage(SAH)remains unclear.The aim of this study was to investigate effects of anti-VEGF therapy on EBI after SAH.C57BL/6 male mice underwent sham or filament perforation SAH modeling,and vehicle or two dosages(0.2 and 1μg)of anti-VEGF antibody were randomly administrated by an intracerebroventricular injection.Neuroscore,brain water content,immunoglobulin G staining,and Western blotting were performed to evaluate EBI at 24~48 h.To confirm the role of VEGF,anti-VEGF receptor(VEGFR)-2(a major receptor of VEGF)antibody was intracerebroventricularly administered and the effects on EBI were evaluated at 24 h.A higher dose,but not a lower dose,of anti-VEGF antibody significantly ameliorated post-SAH neurological impairments and brain edema at 24~48 h post-SAH.Post-SAH bloodbrain barrier disruption was also inhibited by anti-VEGF antibody.The protective effects of anti-VEGF antibody were associated with the inhibition of post-SAH induction of VEGF,VEGFR-2,phosphorylated VEGFR-2,interleukin-1βand a matricellular protein tenascin-C(TNC).Anti-VEGFR-2 antibody also suppressed post-SAH neurological impairments and brain edema associated with VEGFR-2 inactivation and TNC downregulation.These findings demonstrated that VEGF causes post-SAH EBI via VEGFR-2 and TNC and that anti-VEGF therapy is effective for post-SAH EBI.