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Chronic wounds in diabetic condition pose a persistent clinical challenge, primarily due
to impaired cellular energy metabolism and delayed tissue regeneration. Mitochondrial
dysfunction plays pivotal role in this impaired healing process, making mitochondrial
transplantation (MT) a promising therapeutic strategy. This study investigates the
efficacy of MT in accelerating wound repair using a diabetic mice model. Full-thickness
excisional wounds (6mm) were created on the dorsal surface of diabetic mice, followed
by subcutaneous administration of isolated crude mitochondria at low, moderate and
high dose (5ug, 10ug, and 20ug) mitochondria per wound. A vehicle-treated group
receiving phosphate-buffered saline (PBS) served as the control.
Mitochondrial viability and quantification were assessed using MTT assay and Bradford
in wound contraction. Wound closure analysis revealed a dose-dependent acceleration of
healing, with high-dose group exhibiting the most significant improvement in wound
contraction and re-epithelialization. Histological analysis confirmed enhanced tissue
regeneration in the treatment groups. Furthermore real-time PCR analysis demonstrated a
significant upregulation of RAC1, CDC42, and VEGF in the moderate and high treatment
groups, indicating enhanced cytoskeletal remodeling, cellular migration and
angiogenesis.
These findings highlight the therapeutic potential of crude mitochondrial transplantation
in diabetic wound healing by restoring cellular bioenergetics and promoting tissue repair.
This approach offers a promising regenerative strategy for managing chronic wound and
improving diabetic wound outcomes.