Exosomes derived from bone marrow mesenchymal stem cells facilitate repair of radiation-Induced skin injury by attenuating inflammation and apoptosis.

Radiation-induced skin injury (RISI) refers to injury to the skin resulting from exposure to ionizing radiation, for which current treatment options are limited. Exosomes derived from bone marrow mesenchymal stem cells (BMSCs-Exos) have demonstrated significant potential in tissue repair. This study evaluated the healing efficacy of BMSCs‑Exos in a rat model of RISI. BMSCs-Exos were isolated and delivered via subcutaneous injection into the RISI. Our findings revealed that BMSCs-Exos reduced the wound area and lowered the radiation injury score, thereby indicating their capacity to facilitate RISI healing. Histological analysis revealed that BMSCs-Exos enhanced epidermal repair and collagen deposition. Immunological assays revealed significantly higher CD31 and α‑SMA expression of the BMSCs‑Exos treatment group (EXO) than that of the irradiation group (IR), suggesting that BMSCs-Exos promoted angiogenesis. In the EXO group, there was also a downregulation of CD86, Inducible Nitric Oxide Synthase (INOS), Tumor Necrosis Factor-α (TNF-α) and Interleukin-1β (IL-1β) expression, coupled with an upregulation of Macrophage Mannose Receptor 1 (CD206), Arginase-1 (Arg-1), and Interleukin-10 (IL-10) expression, indicating that BMSCs-Exos can induce macrophage polarization towards the M2 phenotype and suppress inflammation. Additionally, BMSCs-Exos decreased the number of TUNEL-positive cells. Western blot analysis of apoptosis-related proteins showed that BMSCs-Exos increased the Bcl-2 expression and reduced Bax expression and promoted phosphorylation of the Akt signaling pathway, which implied suppression of cellular apoptosis. In summary, our findings demonstrate that BMSCs-Exos promote RISI repair by regulating the inflammatory microenvironment, and inhibiting cell apoptosis.