Aim
The intricate healing process involves distinct sequential and overlapping phases in thermal injury. To maintain the zone of stasis in Jackson's burn wound model, proper wound intervention is essential. The extent of research on the histoarchitecture of thermal wound healing and the application of mesenchymal stem cell (MSC)-free-based therapy is limited. This study aimed to assess the efficacy of MSC-secretome-based hydrogel for treating partial-thickness cutaneous thermal burn wounds. Materials and
Conclusion
The secretome hydrogel significantly improves healing outcomes in partial-thickness cutaneous thermal burn wounds. The administration of secretome hydrogel accelerates the reduction of the residual burn area and promotes fibroblast proliferation and collagen density. The repairment of histo-architecture of the damaged tissue was also observed such as the reduction of burn depth, increased angiogenesis and epidermal scar index while the decreased dermal scar index. Furthermore, the secretome hydrogel can modulate the immunocompetent cells by decreasing the polymorphonuclear and increasing the mononuclear cells. Thus, it effectively and safely substitutes for thermal injury stem cell-free therapeutic approaches. The study focuses on the microscopical evaluation of secretome hydrogel; further research to investigate at the molecular level may be useful in predicting the beneficial effect of secretome hydrogel in accelerating wound healing.
Methods
Eighteen male Wistar rats were divided into three groups, namely the hydrogel base (10 mg), hydrogel secretome (10 mg) and Bioplacenton™ (10 mg) treatment groups. All groups were treated twice a day (morning and evening) for 7 days. Skin tissue samples from the animals were processed for histological evaluation using the formalin-fixed paraffin-embedded method on days 3 and 7.
Results
This study's findings showed that secretome hydrogel expedited thermal burn wound healing, decreasing residual burn area, boosting collagen deposition and angiogenesis, guiding scar formation, and influencing the inflammation response facilitated by polymorphonuclear leukocytes and macrophages.