Objective To investigate the protective effect of geniposide on diabetic skin ulcer and its mechanism. Methods Rats were divided into normal group, model group and geniposide subgroup (Gen-L: 200 mg/kg; Gen-H: 500 mg/kg). The diabetic rats were given normal saline or geniposide by intragastric administration (n = 6). Treatment was administered once a day, and the wound healing and inflammation of each group were recorded every day. After 7 days of treatment for diabetic skin ulcers, the wound area, tissue sections, TUNEL staining and Western blot were used to quantitatively analyze the changes of wound healing, apoptosis and related regulatory protein expression. Results Compared with the model group, geniposide (200 mg/kg and 500 mg/kg) orally could significantly promote the wound healing and increase the contraction of the injured area in diabetic rats. In the study of skin wound apoptosis in diabetic rats, TUNEL staining positive cells in geniposide subgroup were significantly reduced (P<0.05). Geniposide can significantly inhibit skin inflammation and promote wound repair, which may be related to the promotion of PI3K and Akt phosphorylation. Conclusion Geniposide can promote skin wound repair in diabetic rats by inhibiting inflammatory response and apoptosis.