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

Abstract

. 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 streptozotocin (STZ, 55 mg/
kg), and excision wounds were created on the dorsal surface of the foot. bisacurone (25, 50, and 100 µg/kg,
p.o.) was administered for 21 days. Bisacurone (50 and 100 µg/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 µg/kg) treatment. Intraperitoneal administration of STZ caused significant up-regulation in TNF-α and IL-1β, whereas significant
down-regulation in Ang-1 and IGF-1 mRNA expression in wound tissue. However, bisacurone (50 and 100
µg/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 µg/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.