RESUMEN
Polycaprolactone (PCL) is a synthetic polymer with good mechanical properties that are useful to produce biomaterials of clinical application. It can be successfully combined with chitosan, which enhances the biomaterial properties through the modulation of molecular and cellular mechanisms. The objective of this study was to evaluate the effects of the use of electrospun fibrous membranes consisting of polycaprolactone (PCL) or polycaprolactone coated with chitosan and poly(ethylene oxide) (PCL+CHI/PEO) on mouse skin lesions. Sixty four Black-57 mice were divided into PCL and PCL+CHI/PEO groups. A 1 cm2 lesion was made on the animals' backs, and the membranes were sutured in place. The tissues were extracted on the 3rd, 7th, and 14th days after the lesion. The tissues were analyzed by histology with Hematoxylin and Eosin (H&E) and Sirius Red stains, morphometry, immunohistochemistry, and Western blot. On the 3rd, 6th, and 9th days after the lesion, the PCL+CHI/PEO group showed a higher wound-healing rate (WHR). On the 3 day, the PCL+CHI/PEO group showed a greater amount of inflammatory infiltrate, greater expression of proliferating cell nuclear antigen (PCNA), and smooth muscle actin (α-SMA) (p < 0.05) compared to the PCL group. On the 7th day after the lesion, the PCL+CHI/PEO group showed a greater amount of inflammatory infiltrate, expression of Tumor Necrosis Factor (TNF-α) and PCNA (p < 0.05). In addition, it showed a greater immunolabeling of Monocyte Chemoattractant Protein-1 (MCP-1) and deposition of collagen fibers compared to the PCL group. The PCL+CHI/PEO membrane modulated the increase in the inflammatory infiltrate, the expression of MCP-1, PCNA, and α-SMA in lesions of mice.
RESUMEN
Pressure ulcers (PrUs)* are chronic wounds caused by a combination of factors, such as repetitive ischemia perfusion injury, bacterial colonization of the wound bed, local tissue hypoxia, or an altered cellular and systemic stress response. The objectives of this study were to analyze fragments of devitalized tissue of Stages III and IV PrUs and compare them with healthy tissue to evaluate the expression of the genes involved in wound inflammation. Samples of healthy skin from patients undergoing plastic surgery (n = 3) were collected, as well as from patients with devitalized tissue from Stages III and IV PrUs (n = 3) by means of sharp debridement. Gene expression analysis identified 5 up-regulated genes and 6 down-regulated genes in the devitalized tissue. Fibroblast cultures treated with devitalized tissue extract showed less attraction and cellular growth compared with the control group. Western blotting analysis showed a tendency of 3 particular genes to decrease in cell cultures treated with devitalized tissue extract. This study demonstrates that all of these mediators stimulate and promote inflammation in the wound bed and that a better understanding of the mechanisms of chronic wound development could lead to novel therapeutic strategies.
