Exogenous Irisin Repair Skin Wounds in Streptozotocin-induced Diabetic Mice Through the AMPK–NF-κB Signaling Pathway

Background Diabetic foot ulcer, a severe complication occurring in diabetic patients, lacks effective remedies at present. Objectives The objective of this research is to investigate the impacts of exogenous irisin on diabetic wounds in mice and explore the associated mechanisms. Materials and Methods An animal model was constructed by administration of streptozotocin (STZ) (50 mg/kg) in mice to simulate a diabetic condition. A full-thickness excisional wound was produced on the dorsal skin of the mice to create a wound for the observation of the wound healing process. Cutaneous administration of 0.1 mL of exogenous irisin solution (1 µg/mL and 3 µg/mL) was applied to the injured tissue to assess the impact of exogenous irisin on the wound. Hematoxylin and eosin (H&E) staining assay was applied to evaluate histological changes in the skin tissue. The expression levels of endogenous irisin, adenosine 5′-monophosphate-activated protein kinase (AMPK), nuclear factor kappa B (NF-κB), and inflammatory factors in the skin tissue of the mice were measured by enzyme-linked immunosorbent assay (ELISA). Results The results showed that irisin levels are positively correlated with the progress of wound healing. The STZ mice exhibited decreased pAMPK, increased NF-κB, and increased inflammatory cytokines. Exogenous irisin treatment restored these abnormal expressions in STZ mice. However, co-treatment with the AMPK inhibitor, Compound C, abolished exogenous irisin’s function of promoting wound healing and relieving inflammation. Conclusion Taken together, exogenous irisin possesses a therapeutic effect on skin wounds in STZ-induced diabetic mice, which is related to the regulation of inflammatory factors mediated by the AMPK–NF-κB pathway.