Exogenous nitric oxide donors such as DETA NONOate, spontaneously release nitric oxide. This study aimed to investigate the effect of DETA NONOate as a nitric oxide releasing drug on the rate of collagen synthesis during the impaired wound healing in a rat model of diabetes. Twelve male Sprague–Dawley rats were transferred into separate metabolic cages. Nine days before wounding, the rats were injected intraperitoneally with streptozotocin (STZ; 55 mg/kg body weight in citrate buffer 0.1 mol/L, pH 4.5) to induce diabetes. The dorsal surface of each rat was properly shaved and a full thickness dermal wound was made. The test group (n=6) was treated with 100 ?M DETA NONOate in phosphate buffer while the control wounds (n=6) received sterile saline (PBS) only on the same day as wounding and every three days for one week. After the skin incision, polyvinyl alcohol (PVA) sponges were implanted subcutaneously on the dorsal of each animal under sterile conditions for the collection of wound fluid. Electrophoresis (current: 20 mA) was performed on the wound fluid. The gel was stained with Coomassie blue G-250, destained, and photographed. DETA NONOate treatment increased the rate of collagen synthesis in the diabetic test group compared to the control group. The nitric oxide donor, DETA NONOate, may represent a potential treatment for impaired wound healing in diabetes by increasing the collagen synthesis at the wound site.