Fig. 4

The H&E-stained skin sections revealed that PRP+ADSC-treatment accelerate the diabetic wound healing: A group I (unwounded group) showed the normal epidermis (E) and dermis with its papillary (P) and reticular (R) layers. B Group II (wounded and non-diabetic group); IIa showed the thin epidermis (E) with inflammatory cell infiltration (I) in papillary layer (P). C Group IIb showed near-normal epidermis (E) and dermis with its papillary (P) and reticular layers (R). D, E Group III (diabetic group) showed the interrupted epidermis with and disorganized keratinocytes with vacuolated cytoplasm (V) and absence of keratin, wound beds were covered by a single layer of squamous cells (curved arrow). The dermis showed a massive inflammatory infiltration, and minimal fine collagen deposition (arrow) with areas of deficient collagen deposition (asterisk). The reticular (R) layer has thick collagen bundles (bold arrow). F–K All treated groups (DM+ PRP group, DM+ADSC group, and DM+ADSCs +PRP group): showed intact epidermis (E) with keratohyalin granules and keratin with papillary (P) layer showed fine collagen fibers (arrow), and blood capillaries (arrowhead). The reticular (R) layer has thick collagen bundles (bold arrow). l Epidermal thickness of the different experimental groups. n = 7 per group. Data are expressed as median (maximum and minimum), **significant compared to the control group at p<0.01, ^$$significant compared to the Sham group at p<0.01, ^##significant compared to the diabetic group at p<0.01, ^££significant compared to groups IV and V at p<0.01, ~significant compared to group V at p<0.05, and ~~significant compared to group IV at p<0.01