摘要： BACKGROUND AND PURPOSE Age-related macular degeneration (AMD) is a complex multifactorial neurodegenerative disease treated by anti-VEGF intravitreal injections. As inflammation has a potential pathological role in retinal degeneration, the pro-inflammatory kallikrein-kinin system might be a relevant alternative pharmacological target. The present study investigated the effects of anti-VEGF and anti-B1R treatments on the inflammatory mechanisms in a rat model of choroidal neovascularization (CNV). EXPERIMENTAL APPROACH Immediately after laser-induced CNV, Long-Evans rats were treated by eye-drop application of a B1R antagonist (R-954) or by intravitreal injection of B1R siRNA or anti-VEGF antibodies. The impact of treatments on gene expression of inflammatory mediators, CNV lesion regression, and the integrity of the blood-retinal barrier was measured ten days later in the retina. B1R and VEGF-R2 cellular localization was also investigated. KEY RESULTS The three treatments had significant inhibitory effects on CNV-induced retina alterations. Anti-VEGF and R-954 significantly alleviated CNV-induced upregulation of B1R, B2R, TNF-α, and ICAM-1. Anti-VEGF additionally reversed the upregulation of VEGF-A, VEGF-R2, HIF-1α, MCP-1 and VCAM-1, whereas R-954 inhibited gene expression of IL-1β and COX-2. Enhanced retinal vascular permeability was abolished by anti-VEGF and significantly reduced by R-954 and B1R siRNA treatments. Leukocyte adhesion was also impaired by anti-VEGF and B1R inhibition. B1R occurred on astrocytes and endothelial cells. CONCLUSION AND IMPLICATIONS B1R and VEGF pathways are both involved in retinal inflammation and damage in laser-induced CNV. The non-invasive and self-administration of B1R antagonists on the surface of the cornea by eye-drops might be an important asset for the treatment of AMD.