Fig. 5: Accelerated diabetic wound healing of porcine by PCD.

a Schematic illustration of the study design. b Blood glucose of normal and diabetic mice before operation (n = 6). c Confocal laser scanning microscope (CLSM) images of wound regions of normal and diabetic mice stained with DHE (images are representative of 3 biologically independent samples). Scale bar: 200 μm. d Representative images of the wound area after the mice received different treatments on Day 0, 3, 7, 9, and 12 (n = 5 biologically independent samples). Scale bar: 5 mm. e Wound area changes in diabetic mice by time (n = 5 biologically independent samples). f CLSM images of wound regions in different treatments stained with DHE (n = 3 biologically independent samples). Scale bar: 200 μm. g The relative mRNA expression levels of proinflammatory cytokine in the wound homogenates of mice (n = 3 biologically independent samples). h Masson staining of wound tissue with different treatments on Day 12 (images are representative of 3 biologically independent samples). Scale bar: 100 μm. i Representative images of the blood vessel CD31-positive endothelial cells (black triangle) analyzed by immunohistochemistry (n = 3 biologically independent samples). Scale bar: 100 μm. j, k The relative mRNA expression levels of VEGFA (j) and collagen deposition-related genes α-SMA (k) in the wound homogenates of mice (CS group: n = 3 biologically independent samples; CA film and CN film groups: n = 3 biologically independent samples; Ctrl, Clinical, and PCD groups: n = 5 biologically independent samples). All data were presented as the mean ± SEM. Statistical significance was determined using a one-way ANOVA test followed by Tukey’s multiple comparison analysis. Parts of a were created with BioRender.com.