Preclinical study demonstrates accelerated diabetic wound healing via bone marrow stem cell mobilization in rabbits, indicating therapeutic potential for refractory ulcers.
Key Points
Investigate the therapeutic mechanism of tibial cortex transverse transport on diabetic foot ulcer healing, focusing on stem cell mobilization and the Wnt/β-catenin signaling pathway.
Established a diabetic foot ulcer model in New Zealand White rabbits using streptozotocin (STZ) and performed tibial cortex transverse transport (TTT) surgery.
Assessed wound healing, tissue regeneration, and neovascularization using macroscopic imaging, histology (H&E and Masson’s trichrome), high-resolution X-ray angiography, and immunofluorescence.
Quantified bone marrow-derived mesenchymal stem cell (BMSC) mobilization, angiogenic factors (SDF-1α, CXCR4, VEGF, Ang2), and Wnt/β-catenin pathway activity using flow cytometry, ELISA, qRT-PCR, and Western blot.
TTT significantly accelerated wound closure and enhanced epidermal and dermal restoration along with collagen deposition.
Neovascularization in wound tissues was markedly elevated alongside increases in circulating BMSC mobilization and homing factors.
TTT stimulated the Wnt/β-catenin pathway in BMSCs, and experimental inhibition of this pathway suppressed TTT-driven stem cell mobilization and tissue regeneration.