Objective Astragalus polysaccharide (APS) has promoting angiogenesis function. To explore the effects of APS collagen sponge on enhancing angiogenesis and collagen synthesis so as to provide evidence for the future tissue engineering appl ication as a kind of angiogenic scaffold. Methods APS collagen sponges were prepared by covalent binding with collagen polypeptides by using of crossl inking agents at the ratio of 1 ∶ 1 (W/W). Twenty 10-week-old SpragueDawley rats (10 males and 10 females, and weighing 200-250 g) were selected. Longitudinal incision was made at both sides of the back to form subcutaneous pockets. APS collagen sponges of 5 mm × 5 mm × 5 mm at size were implanted into the left pockets as the experimental group, collagen sponges without APS of the same size into the right pockets as the control group. The general conditions were observed after operation. At 3, 7, 14，and 21 days, 5 rats were sacrificed and the samples were harvested to count the number of microvessels, to measure the contents of the hydroxyprol ine (Hyp), and to detect the mRNA expressions of angiopoetin 1 (Ang1), matrix metalloproteinases 9 (MMP-9), and tissue inhibitors of metalloproteinases 1 (TIMP-1). Results All rats were al ive during experiment period. The number of microvessels increased gradually, and reached the peak at 14 days in 2 groups; the expermental group was significantly higher than the control group (P lt; 0.05). The contents of Hyp increased gradually in 2 groups, and the experimental group was significantly higher than the control group (P lt; 0.05). The mRNA expressions of Ang1 and MMP-9 in the experimental group were significantly higher than those in the control group at 3, 7, and 14 days (P lt; 0.05); the mRNA expression of TIMP-1 in the experimental group was significantly lower than that in the control group at 3 days and was significantly higher at 14 and 21 days (P lt; 0.05). Conclusion The APS collagen sponges can improve angiogenesis and collagen synthesis in wound heal ing by regulating the expressions of Ang1, MMP-9, and TIMP-1.