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Article Abstract
Background: Diabetic foot ulcer (DFU) is a common and challenging chronic disease that can lead to non-traumatic amputation. Studies have indicated that complex cellular environments in DFU often lead to the dysfunction of several cells at the wound site; however, the mechanism of this injury is still difficult to elucidate.
Methods: DFU and normal skin tissue from patients were analyzed by pathological examination using hematoxylin and eosin (H&E), Masson, myeloperoxidase (MPO) and 8-Oxo-2'-deoxyguanosine (8OHdG) immunohistochemical staining. Extract and identify adipose-derived stem cell (ADSC) exosomes from ADSC culture medium. A diabetic wound healing model and a high-glucose-induced fibroblast cell model were used to analyze the effects of ADSC exosomes on DFU wound healing. In addition, collagen synthesis and fibrosis-related molecules as well as oxidative stress-related indices were detected in the cell model. To uncover the underlying mechanism, we further detected the expression of antioxidant related molecules, including Kelch-like ECH-associated protein 1 (Keap1), nuclear factor erythroid 2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), and glutathione peroxidase 4 (GPX4).
Results: Pathological examination confirmed that DFU tissue displayed increased inflammatory cell infiltration and cell injury compared to normal skin. We confirmed that ADSC exosomes accelerated DFU wound healing and improved collagen synthesis and deposition. ADSC exosomes could reverse high glucose induced fibroblast damage, as well as the ability of collagen synthesis. Furthermore, our results indicated that ADSC exosomes improved HG-induced oxidative stress injury by regulating the expression of the Keap1/Nrf2 axis.
Conclusions: This study revealed that ADSC exosomes alleviated HG-induced fibroblast injury and accelerated diabetic wound healing by regulating the expression of the Keap1/Nrf2 axis.
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| http://dx.doi.org/10.1016/j.cellsig.2025.111936 | DOI Listing |
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