Bisacurone Accelerated Wound Healing in Diabetic Foot Ulcer in Experimental Rats via Activation of Angiogenesis

Diabetic foot ulcers (DFU) are refractory chronic ulcer diseases and seriously affect the prognosis of the disease. Bisacurone has been documented for anti-inflammatory and antioxidant potential. The objective of the present investigation was to evaluate the wound healing activity of bisacurone on DFU. Diabetes was induced in Sprague Dawley rats by intraperitoneal administration of streptozotocm (STZ, 55 mg/kg), and excision wounds were created on the dorsal surface of the foot. bisacurone (25, 50, and 100 mu g/kg, p.o.) was administered for 21 days. Bisacurone (50 and 100 mu g/kg) showed a significant decrease (p < 0.05) in blood glucose, wound area, whereas the rate of wound contraction significantly (p < 0.05) increased as compared to DWC group animals. The STZ-induced decrease in SOD and GSH levels, as well as elevated MDA and NO levels, were significantly (p < 0.05) attenuated by bisacurone (50 and 100 mu g/kg) treatment. Intraperitoneal administration of STZ caused significant up-regulation in TNF-alpha and IL-1 beta, whereas significant down-regulation in Ang-1 and IGF-1 mRNA expression in wound tissue. However, bisacurone (50 and 100 mu g/kg) treatment showed significant (p < 0.05) amelioration in these mRNA expressions. The STZ-induced alteration in would architecture was significantly attenuated (p < 0.05) by bisacurone (50 and 100 mu g/kg) treatment. Bisacurone effectively accelerated wound healing in diabetic rats by inhibiting hyperglycemia, oxidative stress, and inflammation to improve angiogenesis. Thus, bisacurone can be considered a potential therapeutic moiety for managing diabetic foot ulcers.