Wound Healing Activity of Phage-Sisplayed TGF-β1 Model Peptide in Streptozotocin-Induced Diabetic Rats

Objective To evaluate the effect of phage-displayed TGF-beta 1 model peptide on cutaneous wound healing in streptozotocin-induced diabetic rats. Methods Full-thickness excisional wounds were made on the dorsums of 50 rats which were then randomly divided into five groups: negative control group (normal saline (NS)), two TGF-beta 1 control groups which were respectively treated with low-dose TGF-beta 1 ( 5 ng/ml) and high-dose TGF-beta 1 (50 ng/ml), and two model-peptide-treated groups which were respectively treated with low-dose model peptide ( 5 ng/ml,) and high-dose model peptide (50 ng/ml). At day 14 post-injury, rats were euthanised and wounds were assessed by gross, histopathology, immunohistochemistry, immunofluorescence and quantificational real-time polymerase chain reaction. Results A significant increase in rate of wound closure was observed in model peptide groups in comparison to negative control group. The results of histopathological staining revealed that re-epithelization and collagen deposition in model-peptide-treated groups were significantly higher than those in negative control group. The results of immunohistochemistry and immunofluorescence tests showed that Ki67-positive, VEGFA-positive, CD31-positive, alpha-SMA-positive, CD206-positive cells in model peptide and TGF-beta 1 control groups were more than those in negative control group. Furthermore, comparing with the mRNA expression profile in negative control groups, mRNA expression profile in model peptide group showed a decrease in proinflammatory cytokine and an increase in anti-inflammatory cytokine and collagen. Conclusions Phage-displayed TGF-beta 1 peptide facilitates wound healing through accelerating re-epithelialization, enhancing collagen deposition, promoting neo-vascularization, and inhibiting inflammatory response. Model peptide possesses the potential to be a promising treatment strategy for enhancing diabetic wound repair.