ADSC-derived exosomes mitigate radiation-induced skin injury by reducing oxidative stress, inflammation and cell death.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• 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)

Background Radiation-induced skin injury (RISI) is a significant complication of radiotherapy and affects over 95% of patients who undergo radiation treatment. The pathophysiological cascade of RISI includes oxidative stress, persistent inflammation, and excessive fibrotic remodeling. Current treatments provide limited efficacy and primarily focusing on symptomatic relief. Exosomes from adipose-derived stem cells (ADSC-Exo) offer promising therapeutic effects on multiple types of skin injury, while their roles in the treatment of RISI remains to be fully explored. Method A mouse model of RISI and an in vitro radiation-induced cellular damage model were established to evaluate the therapeutic effects of ADSC-derived exosomes. ADSC-Exo were isolated via size-exclusion chromatography and characterized using TEM, NTA, and immunoblotting. H&E staining and Masson staining were used to evaluate the extent of skin radiation-induced skin damage and fibrosis. Skin immunofluorescence was performed to assess macrophage infiltration and polarization, while immunohistochemistry staining was conducted to determine the expression levels of inflammatory mediators in the skin samples. In the in vitro experiments, ROS probes were used to evaluate cellular oxidative stress levels, and western blot analysis was employed to detect the expression levels of apoptosis and pyroptosis related proteins. R

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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