A pathological study of skin wound healing in type II diabetes model mouse
The purpose of this study was to elucidate mechanism of wound healing delay. Full thickness skin wounds were created to both normal and type II diabetes mellitus model mice female BKS.Cg-+Leprdb/+Leprdb/Jcl (db/db mice, mean body weight 40g). Both db/db and normal mice were divided into these groups such as 0, 3 and 7 days after operation.
At 0 day, db/db and normal mice skin wounds were created and sacrificed straight away. Histopathologically, hematoxylin-eosin staining showed slightly inflammatory response characterized mainly by neutrophils was recognized, around the edge of the wound of db/db and normal mice.
At 3 days after operation, db/db and normal mice were sacrificed. Histopathologically, necrosis was observed in the wound area. Moderate amount of inflammatory cells, mainly neutrophils were found. Capillary dilatation was also identified in db/db mice. Granulation tissue formation in db/db mice was unremarkable in comparison with normal mice.
At 7 days after operation, neutrophils were still the main inflammatory cells observed under the regenerated epidermis of db/db mice. As for the normal mice, the regenerated epidermis almost covered the wound area. Histopathologically, using toluidine blue pH2.5, the mast cells were seen in the wound area. The peak of mast cells number was significantly different between db/db and normal mice on each time after operation, indicating a delay of the wound healing in db/db mice (Welch’s t-test).
Immunohistochemically, increase of iNOS-positive fibroblasts was observed in wound area of db/db mice compared with that of normal mice.
From these results, the delay of the wound healing in db/db mice was closely associated with typeIallergic reaction, by increased mast cells and elongation of the state of purulent inflammation.
In addition, the appearance of the mast cells and iNOS-positive fibroblasts might be related to inhibit fibrogenesis during wound healing of the skin in db/db mice.