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Objective: To investigate the angiogenesis changes caused by biodegradable material polycaprolactone/β-tricalcium phosphate (PCL/β-TCP) through the regulation of macrophage polarization, and to provide a basis for its clinical application. Methods: The samples were prepared by 3D printing technology and characterized. In vivo experiments, SD rats were implanted in distal femur. Immunofluorescences taining was performed to detect the expression of angiogenesis marker CD31 and angiography was used to evaluate the vascular volume in the stent. Pro-inflammatory marker iNOS and anti-inflammatory marker Arg-1 in the scaffold were detected by immunofluorescences taining after implantation. PCL/β-TCP and its effect on angiogenesis through the regulation of macrophage polarization were detected by cellco-culture in vitro. The experiment was divided into two groups, the blank group (Control) and the PCL/β-TCP (PT5) group. Macrophage cell line Raw264.7 was inoculated on the surface of the material and the polarization and secretion changes were detected. The expression of the M1 macrophage marker iNOS and M2 macrophage marker Arg-1 were detected by immunofluorescences taining. The transcription of vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF-BB), M1 macrophage marker CCR-7, and M2 macrophage marker CD206 were detected by RT-qPCR. The secretion of VEGF, TNF-α, PDGF-BB and IL-10 were detected by enzyme-linked immunosorbent assay (ELISA). Transwell migration experiment was used to detect the effect of macrophage secretion on HUVECs migration ability of human umbilical vein endothelial cells stimulated by PCL/β-TCP. Results: In vivo experiments, the volume and expression of CD31 were enhanced ( P <0.001,P<0.001). Expression of inflammatory marker iNOS decreased (P <0.001), while the anti-inflammatory marker Arg-1 increased (P <0.001). Invitrostudy, compared with Control, there was no significant difference in synthesis of inflammatory marker iNOS ( P >0.05), and the synthesis of anti-inflammatory marker Arg-1 increased in PT5( P <0.001). Transcription level of inflammatory marker CCR-7 and TNF-α was decreased ( P <0.01, P<0.01) in PT5, while the transcription of anti-inflammatory markers CD206 and IL-10 were up-regulated ( P <0.001, P<0.001). Transcription of VEGF was down-regulated (P <0.01) in PT5, and PDGF-BB transcription level was up-regulated (P <0.001). Treated with PT5, the secretion level of VEGF decreased ( P <0.01), while the secretion level of PDGF-BB was upregulated ( P <0.01) as well as IL-10 (P <0.001). Compared with Control, the secretion of TNF-α was impaired in PT5 (P <0.05). Under the action of macrophage secretion, HUVECs migration ability and expression of CD31 were enhanced (P <0.001). Conclusion: Bone repair material PCL/β-TCP can promote angiogenesis by regulating the polarization of macrophages towards M2, and can be one of the candidate materials for bone repair materials. [ABSTRACT FROM AUTHOR]