Fig. 3: PTβR2I encapsulated in ROS-responsive gel accelerated wound healing in diabetic mice, with improved keratinocyte migration and hair follicle formation in vivo.

a Timeline of diabetic mouse wound healing. b Representative images of wounds taken from day 0 to day 14. Wounds were created using 5 mm biopsy punches on the dorsal skin of db/db mice and treated with hydrogel and PTβR2I/Gel topically and subcutaneously. c Wound sizes over 14 days course of each treatment. Wound size ratios were normalized to day 0 (n ≥ 6). d Cytokeratin 10 and 14 staining illustrated enhanced keratinocyte migration at days 3, 8, and 14 in the PTβR2I/Gel group, compared with the No treatment group and gel-only group. Scale bar = 500 µm for days 3 and 8. Scale bar = 200 µm for day 14. e Masson’s trichrome stained wound sections on day 8 of no treatment, treatment with gel, and treatment with PTβR2I encapsulated in the gel. Scale bar = 500 µm. f Quantification of epidermal thickness at day 8 (n = 8). g Immunohistochemical (IHC) staining of K14 (red) in the wounded region on day 14. Scale bars = 50 μm. h Hair follicle density in the wounded area at day 14 (n = 5). i–k Representative images of proliferated cells in the wound area at days 3, 8, and 14, were made using anti-Ki67 antibody. Scale bar = 50 μm. l Quantification of proliferated cell (Ki67⁺) density (n = 5). All data are shown as mean ± standard error c or mean ± standard deviation f, h, and l. Data were analyzed by one-way ANOVA with Bonferroni post-test (n.s.p > 0.05, **p < 0.01, ***p < 0.001).