Objective To compare the characteristics of ulcer wound healing in current commonly used C57BL/6J-db/db mouse models of spontaneous gene mutation-induced type 2 diabetes and in C57BL/6J mice with diabetes induced by streptozotocin (STZ), and to provide a basis for related experimental studies on diabetic ulcer in animal models. Methods To establish the mouse models of diabetic ulcer wound, observe the healing time and calculate the wound healing rate at 0, 3, 5, 7, 10, 14 days. Tissue samples were collected at days 7 and 14. HE and Masson staining, and immunohistochemistry (CD31 and PCNA) were used to observe the pathological changes of the wound tissues. Gene expressions of collagen-Ⅲα, fibronectin and α-SMA were detected by fluorescent quantitative analysis. Results The wound healing time of db/db mice was significantly delayed compared with the STZ mice, which was extended from 16.6±0.8 d to 20.2±1.3 d (P<0.001). Compared with the STZ group, the growth of granulation tissue in the db/db group was slow, the length of newly formed epithelium was insufficient, the collagen deposition was disordered, and the wound healing was poor. At 7 days, the expression of CD31 and PCNA was significantly lower in the db/db group (P<0.01), and at 7 and 14 days, the increase of collagen-Ⅲα and α-SMA genes up-regulation was significantly lower in the db/db group than in the STZ group. Conclusions Both the two types of diabetic mice show delayed wound healing. However, compared with the STZ-induced diabetic mice, the gene mutation db/db mice are more suitable for studies of diabetic ulcer wound healing as regarding the extent of the delay and the degree of difficulty of wound healing.