Objective To investigate the effect and potential mechanism of angiopoietin 1 (Ang1) on choroidal neovascularization (CNV) of rats. Methods A total of 30 Norwegian (BN) rats aged 6-8 weeks were randomized into three groups (n=10/group): normal group, model group, and Ang1 treatment group. The normal group was not processed, but the other two groups used multi-wavelength krypton laser to model the eyes of BN rats. We then performed fundus fluorescein angiography 14 days post-surgery. After confirming the success of the surgery, on the next day, the Ang1 treatment group received 200 μg/L Ang1 20 μl through vitreous cavity injection, while the other two groups received an equal volume of saline. After another 10-day, we performed Fundus fluorescein angiography examination, measured the CNV area through choroidal patching using FITC-labeled dextran (FITC-dextran) cardiac perfusion, and observed the retinal-choroidal structure changes of rats by Hematoxylin-eosin staining (HE) staining. We also detected the expression of Ang1, Rap1, GAPRap1, and vascular endothelial-cadherin (VE-cadherin) in the retinal-choroidal-sclera complex by Western blotting. Next, we cultured the rat choroidal vascular endothelial cells (RCVECs). When the cells were in the logarithmic growth phase, we stimulated these cells with vascular endothelial growth factor (VEGF) and cultured them for 24 hours, and divided into negative control group (siRNA-NC group), GAPRap1-siRNA group and GAPRap1-siRNA+Ang1 group. We further transfected cells with siRNA-NC (siRNA-NC group) or GAPRap1 small interfering RNA (GAPRap1-siRNA group and GAPRap1-siRNA+Ang1 group). In the GAPGAPRap1 small interfering RNA transfected cells, 6 hours after transfection, we set aside some cells coculture with 200 μg/L Ang1 (GAPRap1-siRNA+Ang1 group). After another 24 hours, we extracted and quantified the expression levels of GAPRap1, Rap1, and VE-cadherin by Western blotting. We detected the expression of VE-cadherin using immunofluorescence. Results Compared with normal group, in model group, the neovascular leakage area and choroidal damage degree significantly increased (P<0.01), the expression of GAPRap1 and VE-cadherin proteins significantly reduced (P<0.05), and the expression of Rap1 had no significant change (P>0.05). Compared with model group, in the Ang1 treatment group the neovascular leakage area and choroidal damage degree were significantly reduced (P<0.01), the expression of GAPRap1 and VE-cadherin proteins in the choroid and cells significantly increased (P<0.01), the expression of Rap1 had no statistical change (P>0.05). In choroidal tissue, the expression of Ang1 protein in Ang1 treatment group was significantly higher than that in the other two groups (P<0.01). In the cell experiment, the expressions of GAPRap1 and VE-cadherin in GAPRap1-siRNA group were significantly lower than those in the GAPRap1-siRNA+Ang1 group and the siRNA-NC group (P<0.01), while the expression of Rap1 had no significant change (P>0.05). The immunofluorescence results showed that the fluorescence of VE-cadherin in the GAPRap1-siRNA group was significantly lower than that in the GAPRap1-siRNA+Ang1 group and siRNA-NC group (P<0.001). Conclusion Ang1 can reduce the leakage of choroidal neovascularization in rats, which has an inhibitory effect on CNV growth, and its mechanism may be related to the enhancement of cell adhesion through the GAPRap1-VE-cadherin pathway.