Antimicrobial Peptide Buforin-I Facilitates the Healing of Foot Wounds in Diabetic Mice.

BackgroundDiabetic wounds are difficult to heal due to long-term chronic ulcers, thus lacking effective treatment methods. Some antimicrobial peptides are known to have biological functions that promote wound healing, but the effects of the antimicrobial peptide Buforin-I on diabetic wound healing and the mechanisms underlying these effects are not yet elucidated.MethodsThis project investigated the effects of Buforin-I on the healing rate of foot wounds in streptozotocin (STZ)-induced diabetic mice and the antioxidant reactions in wound tissues. Histological staining with HE and Masson, as well as biochemical assays with immunohistochemistry (IHC), were applied to assess tissue chemistry markers. The activity levels of SOD, GSH, and reactive oxygen species (ROS) were measured to evaluate oxidative stress levels. TUNEL analysis was carried out to detect the apoptosis rate. The levels of VEGF, TGF-β1, and Nrf2 were measured by enzyme-linked immunosorbent assay (ELISA) and western blot (WB). In addition, the in vitro effects of Buforin-I on cell proliferation, apoptosis, migration, and oxidative stress levels under high glucose conditions were analyzed on HaCaT cells. Cell viability was measured using an MTT assay, and cell migration was assessed through the wound healing experiment.ResultsBuforin-I treatment accelerated the healing of foot wounds in STZ-induced diabetic mice, with increased fibroblast proliferation and collagen deposition in the wound tissue and decreased Nrf2-mediated oxidative stress levels. Furthermore, Buforin-I facilitated the proliferation and migration as well as reduced apoptosis of HaCaT cells under high glucose conditions, thus enhancing the antioxidant capacity of HaCaT cells.ConclusionIn conclusion, this study confirmed the promoting effect of Buforin-I on diabetic wound healing through the regulation of oxidative stress, highlighting the potential application of Buforin-I in diabetic wound healing.