Objective To investigate the effect of local injection of endostatin on hypertrophic scar of rabbit ear, and explore the mechanism. Methods Models of hypertrophic scar of rabbit ear were established. Four weeks after model establishment, scar tissues of right rabbit ears were injected with endostatin once a week for three weeks (experiment group, n=10), and scar tissues of left rabbit ears were injected with normal saline once a week for three weeks (control group,  n=10). Seven weeks after model establishment, scar tissues of rabbit ears in experiment group and control group were obtained, histomorphological changes were observed with HE staining, expression of microvessel marker CD34 was determined by immunohistochemistry, and apoptosis of fibroblasts was detected by TUNEL. Umbilical endothelial cells were cultured in vitro and seeded on Martrigel culture system with different concentrations of endostatin, and vessel tube formation of endothelial cells was observed. Results Compared with control group, the area of hypertrophic scar in experiment group significantly reduced, the number of fibroblasts in scar tissues decreased and collagen density became loose. The percent of cells with positive expression of CD34 in scar tissues in experiment group was significantly lower than that in control group [(2.21±0.39)% vs (6.11±1.32)%, P<0.05], while the percent of  apoptotic cells in experiment group was significantly higher than that in control group [(9.06±1.54)% vs (5.21±1.11)%, P<0.05]. In vitro observation revealed that more microvessel branches formed in Martrigel culture system without endostatin, and the number of microvessel tube formation gradually decreased with the increase of mass concentration of  endostatin. Conclusion Local injection of endostatin may inhibit hypertrophic scar development and promote scar regression, which may be correlated with the inhibition of microvessel tube formation.