Objective To investigate the protective effect of geniposide against diabetic rats with skin ulcer and the mechanism. Methods Rats were divided into a normal group, model group, and geniposide subgroups (Gen(L): 200 mg/ kg; Gen ( H): 500 mg/ kg). Diabetic rats were treated with normal saline or geniposide by intragastric administration (n=6). Treatments were 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 changes in wound healing, apoptosis, and related regulatory protein expression. Results Compared with the model group, the group receiving orally administered geniposide (200 and 500 mg/ kg) showed significantly improved wound healing and increased contraction of the injured area. In terms of skin wound apoptosis in diabetic rats, TUNEL-positive cells were significantly reduced in geniposide subgroups (P<0. 05). Geniposide significantly inhibited skin inflammation and promoted wound repair, which may be related to promotion of PI3K and Akt phosphorylation. Conclusions Geniposide promoted skin wound repair in diabetic rats by inhibiting inflammatory responses and apoptosis.