ADSC exosomes improve high glucose induced fibroblast oxidative stress injury and accelerate DFU wound healing via regulating Keap1/Nrf2 axis.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

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. 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). 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 improve

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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