Connective tissue research · 2026
Autologous platelet-rich gel promotes diabetic foot ulcer wound healing by activating the Wnt/β-catenin signaling pathway.
СтатьяНазвание и аннотация: Перевод в очереди
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Du Liangliang, Dai Yuwei, Sui Jiayu, Liao Yuwen, Liu Yonghe, Du Liusi, Zeng Douyun
Аннотация
PURPOSE: Diabetic foot ulcers (DFUs), a major cause of disability in diabetic patients, pose a significant clinical challenge. Autologous platelet-rich gel (APG), an advanced biotherapeutic approach, has demonstrated considerable potential in promoting DFU wound healing. This study aimed to investigate the therapeutic mechanisms of APG in DFU.
METHODS: A DFU model was established in streptozotocin-induced Sprague-Dawley rats. Wound closure rates were measured on days 7 and 14 post-injury. Histological evaluation was conducted using hematoxylin and eosin (H&E) staining. The expression of collagen I and III was assessed by immunohistochemistry (IHC). Activation of the Wnt/β-catenin pathway and related signaling molecules (NF-κB, STAT3) was determined by western blot analysis.
RESULTS: APG treatment significantly reduced wound area, enhanced granulation tissue formation and epithelial regeneration, and promoted the expression of collagen I and III. Mechanistically, APG specifically activated the Wnt/β-catenin pathway, as indicated by increased β-catenin protein levels. Importantly, the beneficial effects of APG on wound healing, tissue repair, and collagen deposition were effectively abolished by co-treatment with XAV-939.
CONCLUSIONS: These findings reveal a novel mechanism underlying APG-mediated DFU healing and provide a theoretical foundation for the beneficial role of Wnt/β-catenin signaling in wound repair. This study offers new perspectives and directions for ulcer treatment strategies.
METHODS: A DFU model was established in streptozotocin-induced Sprague-Dawley rats. Wound closure rates were measured on days 7 and 14 post-injury. Histological evaluation was conducted using hematoxylin and eosin (H&E) staining. The expression of collagen I and III was assessed by immunohistochemistry (IHC). Activation of the Wnt/β-catenin pathway and related signaling molecules (NF-κB, STAT3) was determined by western blot analysis.
RESULTS: APG treatment significantly reduced wound area, enhanced granulation tissue formation and epithelial regeneration, and promoted the expression of collagen I and III. Mechanistically, APG specifically activated the Wnt/β-catenin pathway, as indicated by increased β-catenin protein levels. Importantly, the beneficial effects of APG on wound healing, tissue repair, and collagen deposition were effectively abolished by co-treatment with XAV-939.
CONCLUSIONS: These findings reveal a novel mechanism underlying APG-mediated DFU healing and provide a theoretical foundation for the beneficial role of Wnt/β-catenin signaling in wound repair. This study offers new perspectives and directions for ulcer treatment strategies.